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Spastic hypertonia: Mechanisms and measurement
Abstract
Spastic hypertonia has been defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome. Heightened muscle tone may be the result of changes intrinsic to the muscle or to altered reflex properties. Increased motoneuronal excitability and/or enhanced stretch-evoked synaptic excitation of motoneurons are mechanisms that might enhance stretch reflexes. Two distinct parameters may be altered in the pathologic stretch reflex--the "set point," or angular threshold of the stretch reflex, and the reflex "gain," or the amount of force required to extend the limb in proportion to the increasing joint angle. Earlier studies fail to dissociate the contributions of reflex threshold and reflex gain. Recent investigations suggest that spastic hypertonia may be the result of a decrease in stretch reflex threshold without significant increase in reflex gain, as was previously believed. Various clinical scales, biomechanical paradigms, pendulum models, and electrophysiologic studies have been used to quantify spastic hypertonia. Biomechanical methods seem to correlate most closely with the clinical state. Spastic hypertonia is but one component of the upper motor neuron syndrome, whose features also include loss of dexterity, weakness, fatigability, and various reflex release phenomena. These other features of the upper motor neuron syndrome may well be more disabling to the patient than changes in muscle tone.
... Los efectos de la espasticidad son objetivables al nivel espinal segmentario en forma de reflejos tendinosos exagerados o tono muscular aumentado y a nivel funcional como un trastorno del movimiento. [105][106][107][108] Elegir pacientes con daño medular completo como nuestra primera cohorte de pacientes reduciría la complejidad de la evaluación de la espasticidad sólo a métodos desarrollados para exploración segmentaria. ...
... Cada método descripto tiene ventajas, inconvenientes y capacidades de medición únicas. Otras revisiones proporcionan una descripción más com- 105,106,[113][114][115] La mayoría de los métodos tienen como objetivo estimar la excitabilidad del arco reflejo segmentario, una aproximación muy somera de la excitabilidad del conjunto de alfa-motoneuronas. Por ejemplo, tanto en las pruebas biomecánicas como en las electrofisiológicas, se puede establecer un umbral reflejo midiendo la posición del ángulo de la articulación, la profundidad del tendón, la fuerza de la toma o la intensidad de estimulación constante a la que aparece por primera vez el reflejo miotático. ...
... Por ejemplo, tanto en las pruebas biomecánicas como en las electrofisiológicas, se puede establecer un umbral reflejo midiendo la posición del ángulo de la articulación, la profundidad del tendón, la fuerza de la toma o la intensidad de estimulación constante a la que aparece por primera vez el reflejo miotático. Se ha demostrado que el umbral reflejo es una medida confiable del nivel de excitabilidad del bucle segmentario, 105,113,114 por lo tanto, es útil evaluar el umbral segmentario para estimar la eficacia de la estimulación. ...
Introducción: La espasticidad es una condición relacionada a daño cerebral o de la médula espinal que afecta a millones de personas en el mundo, causada a menudo por eventos como accidente cerebro – vascular, daño traumático cerebral o medular, aunque es también común un comienzo insidioso del padecimiento. Sin desmedro de la causa, la espasticidad resultante llevará a años de discapacidad y calidad de vida reducida. Se dispone de varios tratamientos para esta condición mórbida, aunque cada uno de ellos está gravado con inconvenientes, incluyendo respuesta clínica incompleta, alto costo, duración limitada de respuesta, efectos colaterales limitantes relacionados a la dosis, y necesidad de mantenimiento periódico. La estimulación medular (EM), alguna vez promisorio tratamiento para la espasticidad, ha sido relegada a un estado experimental permanente. Métodos.En esta revisión, nuestro objetivo es documentar y criticar la historia y evaluar el desarrollo de SCS como tratamiento de la espasticidad de las extremidades inferiores. Al incorporar los descubrimientos recientes con los conocimientos adquiridos por los primeros pioneros en este campo, tenemos la intención de sentar las bases necesarias para proponer hipótesis comprobables para estudios futuros. Resultados. La EM ha sido probada en más de 25 condiciones diferentes desde que se reportó un efecto potencialmente beneficioso en 1973. Sin embargo, la falta de una comprensión completa de la fisiopatología de la espasticidad, la metodología de estudio arcaica y las limitaciones tecnológicas iniciales del hardware implantable limitan la validez de muchos estudios. SCS ofrece una medida de control de la espasticidad que no se puede reproducir con otras intervenciones. Conclusiones. Con una mejor miniaturización de la fuente de energía, algoritmos de control personalizados, un diseño de implantes más desarrollado y una mayor comprensión de la fisiopatología de la espasticidad estamos preparados para reintroducir y volver a probar la EM en esta población.
... Two of the most widely used assessments are the Modified Ashworth Scale [MAS, (Bohannon and Smith, 1987)] and the Tardieu Scale (Tardieu et al., 1954). Unfortunately, clinical measures, and in particular the MAS, which is the most frequently used scale, lack validity and reliability, as they are subjective and rely heavily on the therapist's experience (Katz and Rymer, 1989;Cha and Arami, 2020;Germanotta et al., 2020). Furthermore, they cannot be performed in unsupervised settings. ...
... We hypothesize that the proposed method would be able to accurately estimate muscle tone/stiffness parameters and capture differences between unimpaired and stroke subjects over exercise time. In the stroke group, we also expect muscle tone parameters to be speed-dependent but not significantly correlated with the MAS due to its limited reliability and resolution (Katz and Rymer, 1989;Melendez-Calderon et al., 2013). This work could be an important step towards developing smart algorithms that automatically adapt therapy parameters to continuously ensure user's safe use of rehabilitation robots during unsupervised therapy. ...
... 11 patient (i.e., therapy task and adaptation depending on their muscle tone level) is essential to prevent abnormal muscle tone increase during therapy. The outcome measures of the proposed method did not correlate with the MAS, however this is not surprising given the limited resolution and reliability of the scale, and its differences in assessment paradigm (e.g., single and lower speed, different range of motion) (Katz and Rymer, 1989;Melendez-Calderon et al., 2013). ...
Introduction: Robot-assisted neurorehabilitation is becoming an established method to complement conventional therapy after stroke and provide intensive therapy regimes in unsupervised settings (e.g., home rehabilitation). Intensive therapies may temporarily contribute to increasing muscle tone and spasticity, especially in stroke patients presenting tone alterations. If sustained without supervision, such an increase in muscle tone could have negative effects (e.g., functional disability, pain). We propose an online perturbation-based method that monitors finger muscle tone during unsupervised robot-assisted hand therapy exercises.
Methods: We used the ReHandyBot, a novel 2 degrees of freedom (DOF) haptic device to perform robot-assisted therapy exercises training hand grasping (i.e., flexion-extension of the fingers) and forearm pronosupination. The tone estimation method consisted of fast (150 ms) and slow (250 ms) 20 mm ramp-and-hold perturbations on the grasping DOF, which were applied during the exercises to stretch the finger flexors. The perturbation-induced peak force at the finger pads was used to compute tone. In this work, we evaluated the method performance in a stiffness identification experiment with springs (0.97 and 1.57 N/mm), which simulated the stiffness of a human hand, and in a pilot study with subjects with increased muscle tone after stroke and unimpaired, which performed one active sensorimotor exercise embedding the tone monitoring method.
Results: The method accurately estimates forces with root mean square percentage errors of 3.8% and 11.3% for the soft and stiff spring, respectively. In the pilot study, six chronic ischemic stroke patients [141.8 (56.7) months after stroke, 64.3 (9.5) years old, expressed as mean (std)] and ten unimpaired subjects [59.9 (6.1) years old] were tested without adverse events. The average reaction force at the level of the fingertip during slow and fast perturbations in the exercise were respectively 10.7 (5.6) N and 13.7 (5.6) N for the patients and 5.8 (4.2) N and 6.8 (5.1) N for the unimpaired subjects.
Discussion: The proposed method estimates reaction forces of physical springs accurately, and captures online increased reaction forces in persons with stroke compared to unimpaired subjects within unsupervised human-robot interactions. In the future, the identified range of muscle tone increase after stroke could be used to customize therapy for each subject and maintain safety during intensive robot-assisted rehabilitation.
... Ocorrendo numa variedade de desordens do sistema nervoso central, a presença de espasticidade tem significância tanto diagnóstica quanto terapêutica. A presença de resistência durante a movimentação passiva é freqüentemente utilizada para quantificar o tônus muscular 2,3 . Contudo, vários fatores contribuem para o aumento da resistência à movimentação passiva observada em pacientes espásticos 1,2 e uma diferenciação entre as tensões causada pela espasticidade e pelas propriedades viscoelásticas dos tecidos moles nem sempre é possível 1,2,4 , induzindo a planos de tratamento inapropriados. ...
... Uma definição amplamente aceita de espasticidade é a de que é uma desordem motora caracterizada por um aumento da resistência ao movimento passivo dependente da velocidade de alongamento, associada com hiper-reflexia e resultado de uma hiperexcitabilidade do reflexo miotático 2,[5][6][7][8] . Espasticidade pode causar alterações musculares secundárias e desenvolvimento de contraturas. ...
... Escalas clínicas, como a escala de Ashworth, podem não ser sensíveis o suficiente para detectar alterações discretas de tônus 1,6,11,14 . Métodos biomecânicos envolvem equipamentos caros, requerem recursos humanos especializados e nem sempre podem ser disponíveis para aplicações em rotinas clínicas 1,5,11,[14][15][16][17][18][19] e os métodos neurofisiológicos apresentam uma fraca correlação com o status clínico da espasticidade 2,5,20 . ...
Objetivo deste estudo foi investigar a confiabilidade do teste de pêndulo para avaliar o tônus muscular e comparar os dados obtidos entre um grupo de idosos saudáveis e um grupo de pacientes hemiplégicos crônicos da mesma faixa etária. Vinte idosos e 20 hemiplégicos crônicos foram recrutados na comunidade, de forma voluntária. O tônus muscular foi investigado utilizando o índice de relaxamento corrigido (IRC) obtido pelo teste de pêndulo. Para avaliar a confiabilidade do IRC, os dados foram obtidos em dois dias diferentes para ambos os grupos. Testes-t foram empregados para avaliar diferenças entre os grupos e entre os lados afetado e não afetado do grupo hemiplégico. A média do IRC para o lado afetado foi 0,65 (± 0,20) no primeiro dia e 0,66 (± 0,11) no segundo dia. Para o lado não afetado, as médias foram 1,03 (± 0,09) e 1,02 (± 0,11) para os primeiro e segundo dias, respectivamente. Coeficientes de correlação significativos foram observados entre as duas medidas obtidas (r = 0,93 e r = 0,70) para os lados afetado e não afetado, respectivamente. Os resultados do teste-t demonstraram diferenças significativas entre os valores do IRC obtidos no lado afetado comparados com os valores do lado não afetado e os valores de referência. Entretanto, não foram observadas diferenças significativas entre os valores do IRC obtidos no lado não afetado e os valores de referência. Pode-se concluir que o teste de pêndulo apresenta o potencial de ser incluído como um método eficaz de medida de tônus muscular em reabilitação.
... 3 Increased muscle tone in patients with upper motor neuron syndrome can be attributed to 2 causes: intrinsic muscle stiffness or an increase in the tonic stretch reflex (spasticity). 3,4 Valid and reliable outcome measures are needed to quantify the severity of spasticity. 5 Despite questionable validity and inconsistent reliability, the Modified Ashworth Scale (MAS) is the most commonly used outcome measure to assess spasticity in clinical settings. ...
... 5,6 A disadvantage of this test is that it cannot distinguish the neurologic origin of spasticity (resistance due to a hyperactive tonic stretch reflex) from a mechanical origin of spasticity (resistance due to increased intrinsic muscle stiffness). 3,4,8,9 Bohannon and Smith 10 originally reported the interrater reliability of the MAS in a mixed sample of patients with central Disclosures. None. ...
... 3 Increased muscle tone in patients with upper motor neuron syndrome can be attributed to 2 causes: intrinsic muscle stiffness or an increase in the tonic stretch reflex (spasticity). 3,4 Valid and reliable outcome measures are needed to quantify the severity of spasticity. 5 Despite questionable validity and inconsistent reliability, the Modified Ashworth Scale (MAS) is the most commonly used outcome measure to assess spasticity in clinical settings. ...
... 5,6 A disadvantage of this test is that it cannot distinguish the neurologic origin of spasticity (resistance due to a hyperactive tonic stretch reflex) from a mechanical origin of spasticity (resistance due to increased intrinsic muscle stiffness). 3,4,8,9 Bohannon and Smith 10 originally reported the interrater reliability of the MAS in a mixed sample of patients with central Disclosures. None. ...
Objective:
To evaluate the reliability of the protocol for administration of MAS for all commonly affected muscle groups after stroke.
Design:
Repeated-measures design was used in administration of MAS for 13 muscle groups on two assessment days. Intrarater reliability and interrater reliability (between three raters) was assessed.
Setting:
Inpatient rehabilitation.
Participants:
30 patients, 1-19 months after stroke (age 55.1 ± 13.5 years).
Interventions:
Not applicable.
Main outcome measure:
Intra- and interrater reliability of the muscle tone assessment protocol with MAS for 7 upper- and 6 lower-limb muscle groups compiled from previous studies; one modified and four originally described. The weighted kappa was calculated.
Results:
The most and the least frequently assigned MAS grade was 0 and 4, respectively. Agreement was the highest for grade 0 (49% within; 32% between raters). Intrarater reliability was good to excellent for upper limb- (κ 0.71-0.94) and moderate to excellent for lower limb muscles (κ 0.55-0.97). Interrater reliability was poor to good for upper limb- (κ 0.25-0.66) and moderate for lower limb muscles (κ 0.41-0.54).
Conclusion:
The intrarater reliability of MAS was moderate for the hip flexors. The reliability results for the other 4 muscles studied anew after stroke were similar to the predetermined ones. The better intrarater reliability results confirmed previous findings. Due to lower interrater reliability, caution is needed in interpreting the results when reassessment is not possible by the same examiner. A well-described protocol for administering the MAS may lead to its standardization.
... Cerebral palsy is the most common childhood motor disability [287][288][289][290], with~80% of clinical presentations involving spasticity (sCP) [38, 290,291]. Despite the aetiology of sCP being a topic of intense debate [38, [292][293][294][295][296][297][298][299], the symptoms, therapeutic interventions and the timing of syndrome onset is consistent with a major influence of inhibitory neurotransmission on sCP [300,301]. Symptomatically, cerebral palsy is characterized by spasticity (sCP), dyskinesias, ataxia, hyper-reflexia and occasionally hypotonia [290,302,303]. Notably, spasticity and hypertonia, defined clinically as the resistance of a muscle to stretch [304][305][306]. ...
... Notably, spasticity and hypertonia, defined clinically as the resistance of a muscle to stretch [304][305][306]. and hyper-reflexia, increased stretch reflex responses, are thought to involve specific disinhibitory mechanisms [300,301,307,308]. Moreover, the timing of the development of the sCP syndrome is concomitant with the postnatal maturation of chloride channels (NKCC1 to KCC2-see above) throughout the neuraxis [163,309,310]. ...
During development, GABA and glycine play major trophic and synaptic roles in the establishment of the neuromotor system. In this review, we summarise the formation, function and maturation of GABAergic and glycinergic synapses within neuromotor circuits during development. We take special care to discuss the differences in limb and respiratory neuromotor control. We then investigate the influences that GABAergic and glycinergic neurotransmission has on two major developmental neuromotor disorders: Rett syndrome and spastic cerebral palsy. We present these two syndromes in order to contrast the approaches to disease mechanism and therapy. While both conditions have motor dysfunctions at their core, one condition Rett syndrome, despite having myriad symptoms, has scientists focused on the breathing abnormalities and their alleviation—to great clinical advances. By contrast, cerebral palsy remains a scientific quagmire or poor definitions, no widely adopted model and a lack of therapeutic focus. We conclude that the sheer abundance of diversity of inhibitory neurotransmitter targets should provide hope for intractable conditions, particularly those that exhibit broad spectra of dysfunction—such as spastic cerebral palsy and Rett syndrome.
... Additionally, suppose the dominant side is affected post stroke, In that case, individuals can get motivated to use that hand during recovery. In the present study, it is stated that impairment of the dominant hand will affect daily activities more and may cause inconvenience to patients (Katz and Rymer, 1989). ...
Purpose : Stroke is a major cause of mortality and causes significant impairment of functional mobility, regardless of whether it affects the dominant or non-dominant side, can increase future health risks. Our study purpose was to determine the impact of dominance in functional mobility impairment on stroke survivors. Methods: The research was conducted at Krishna College of Physiotherapy, Karad, involving 132 stroke patients, both male and female, with either left or right side affected by stroke. Participants were selected by random sampling based on predefined inclusion and exclusion criteria. They were evaluated using the Functional Independence Measure Scale (FIMS) and the Barthel Index Scale (BI). Collected data were analysed by SPSS version 26.0. Results: The study evaluated about functional mobility impairment on the dominant and non-dominant sides on the 1st and 45th day post-stroke. For Barthel index assessment, group B had significant improvement ( p <0.0001 ) than group A(p<0.2846) There was more improvement of Functional Mobility seen in the group B (p <0.0001) for Functional Independence Measure ) affected Stroke survivors than compared to group A (p 0.0004) for Functional Independence Measure). Between group analysis for post test measurements was (p<0.0001) for both BI and FIMS showing significant differences. Conclusion: This study revealed that, 45 days post-stroke, functional mobility was significantly impaired in survivors of stroke with dominant side affected compared to the non-dominant side.
... Spasticity has traditionally been defined as a motor disorder marked by a velocitydependent increase in tonic stretch reflexes (commonly referred to as muscle tone), often accompanied by exaggerated tendon reflexes. This condition arises from the hyperexcitability of the stretch reflex mechanism [2,3]. Years later, Pandyan et al. [4] expanded this understanding by introducing the concept of spasticity as a sensory-motor disorder, highlighting the interplay between sensory and motor components in its pathophysiology [5]. ...
Stroke is a leading cause of long-term disability worldwide, often resulting in spasticity. Botulinum toxin injections have emerged as a cornerstone in the management of post-stroke spasticity. However, despite their clinical efficacy, maintaining long-term adherence to botulinum toxin therapy remains a significant challenge. This retrospective observational study analyzed 106 patients undergoing botulinum toxin therapy for post-stroke spasticity to identify the key factors influencing treatment continuation. The mean age of the cohort at the time of stroke was 57.7 years, with ischemic strokes accounting for 61.3% of cases and hemorrhagic strokes for 38.7%. A total of 61.3% of patients continued therapy, while 38.7% discontinued therapy due to a variety of reasons. The most common reasons included logistical barriers (43.9%) and comorbidities (36.6%), followed by perceived lack of benefit (24.4%) and clinical resolution (12.2%). Among those citing a lack of benefit, muscular fibrosis was a notable contributor. In the multivariable Cox regression analysis, logistical challenges, such as access to healthcare facilities and administrative difficulties, were associated with discontinuation (HR = 13.95, 95% CI: 5.57–34.94, p < 0.001). Comorbidities also significantly increased the likelihood of discontinuation (HR = 3.51, 95% CI: 1.56–7.87, p = 0.002), as did the lack of benefit (HR = 14.34, 95% CI: 5.65–36.38, p < 0.001) and condition resolution (HR = 19.20, 95% CI: 5.58–66.02, p < 0.001). In contrast, demographic and clinical factors, including age at the time of stroke, gender, stroke type, affected side, and baseline spasticity severity, did not significantly influence treatment continuation. These findings underscore the importance of addressing logistical barriers and mitigating the burden of comorbidities to enhance treatment adherence. A shift toward patient-centered approaches that integrate robust rehabilitation services and streamline healthcare accessibility is critical for optimizing outcomes.
... Spasticity is defined as a "velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex" (32). The excitability of the monosynaptic Ia afferent-motoneuron (MN) pathway, which underlies the stretch reflex is regulated by intricate spinal circuitries, which are in turn modulated by supraspinal pathways descending from cortical and brainstem structures (33). ...
Background
In healthy subjects, repetitive transcranial magnetic stimulation (rTMS) targeting the primary motor cortex (M1) demonstrated plasticity effects contingent on electroencephalography (EEG)-derived excitability states, defined by the phase of the ongoing sensorimotor μ-oscillation. The therapeutic potential of brain state-dependent rTMS in the rehabilitation of upper limb motor impairment post-stroke remains unexplored.
Objective
Proof-of-concept trial to assess the efficacy of rTMS, synchronized to the sensorimotor μ-oscillation, in improving motor impairment and reducing upper-limb spasticity in stroke patients.
Methods
We conducted a parallel group, randomized double-blind controlled trial in 30 chronic stroke patients (clinical trial registration number: NCT05005780). The experimental intervention group received EEG-triggered rTMS of the ipsilesional M1 [1,200 pulses; 0.33 Hz; 100% of the resting motor threshold (RMT)], while the control group received low-frequency rTMS of the contralesional motor cortex (1,200 pulses; 1 Hz, 115% RMT), i.e., an established treatment protocol. Both groups received 12 rTMS sessions (20 min, 3× per week, 4 weeks) followed by 50 min of physiotherapy. The primary outcome measure was the change in upper-extremity Fugl-Meyer assessment (FMA-UE) scores between baseline, immediately post-treatment and 3 months’ follow-up.
Results
Both groups showed significant improvement in the primary outcome measure (FMA-UE) and the secondary outcome measures. This included the reduction in spasticity, measured objectively using the hand-held dynamometer, and enhanced motor function as measured by the Wolf Motor Function Test (WMFT). There were no significant differences between the groups in any of the outcome measures.
Conclusion
The application of brain state-dependent rTMS for rehabilitation in chronic stroke patients is feasible. This pilot study demonstrated that the brain oscillation-synchronized rTMS protocol produced beneficial effects on motor impairment, motor function and spasticity that were comparable to those observed with an established therapeutic rTMS protocol.
Clinical Trial Registration
ClinicalTrials.gov, identifier [NCT05005780].
... This is particularly useful in view of future home therapy applications. Moreover, the robotic assessment is more accurate compared to the MAS, which has limited resolution and reliability [25,48,49]. ...
Upper-limb spasticity, frequent after central nervous system lesions, is typically treated with botulinum neurotoxin type A (BoNT-A) injections to reduce muscle tone and increase range of motion. However, performing adjunct physical therapy post-BoNT-A can be challenging due to residual weakness or spasticity. This study evaluates the feasibility of hand therapy using a robotic hand orthosis (RELab tenoexo) with a mobile phone application as an adjunct to BoNT-A injections. Five chronic spastic patients participated in a two-session pilot study. Functional (Box and Block Test (BBT), Action Research Arm Test (ARAT)), and muscle tone (Modified Ashworth Scale (MAS)) assessments were conducted to assess functional abilities and impairment, along with usability evaluations. In the first session, subjects received BoNT-A injections, and then they performed a simulated unsupervised therapy session with the RELab tenoexo in a second session a month later. Results showed that BoNT-A reduced muscle tone (from 12.2 to 7.4 MAS points). The addition of RELab tenoexo therapy was safe, led to functional improvements in four subjects (two-cube increase in BBT as well as 2.8 points in grasp and 1.3 points in grip on ARAT). Usability results indicate that, with minor improvements, adjunct RELab tenoexo therapy could enhance therapy doses and, potentially, long-term outcomes.
... Over-excitation of α-motor neurons is the main manifestation of spinal cord changes in stroke patients with spasticity. 13 The peripheral mechanism is mainly the change of muscle mechanical properties, 14 that is, the inherent properties and muscle metabolism and function of the tissues that make up muscles, tendons, joints, and other structures. To further explore the mechanism of spasticity after stroke, Mirbagheri et al. 15 found in an observation of the mechanical properties of elbows of patients with muscle spasms after stroke that the spasticity mechanism gradually transitioned over time from neurological factors to peripheral mediated factors. ...
Lower limb spasticity and clonus are common sequelae after cerebral stroke. An important part of their etiopathogenesis has been related to the peripheral component of spasticity. Rheological properties of the tissues seem to be involved. Several studies highlighted anatomical and functional changes in the connective structures. The fasciae might be implicated in the pathological process. Thus, this study intends to investigate the effect of the Fascial Manipulation (FM) technique on triceps surae in stroke patients through a clinical randomized controlled trial, to provide a reference for clinical treatment of lower limb spasticity and ankle clonus. A total of 40 patients with post-stroke ankle clonus were selected and divided into a control group and an observation group by random number table method, with 20 cases in each group. Both groups received conventional rehabilitation therapy, while the FM group received Fascial Manipulation based on conventional rehabilitation therapy. Before the first treatment and after 3 weeks of treatment, the Comprehensive Spasticity Scale (CSS), the Passive Range Of Motion (PROM), the simplified Fugl-Meyer motor function score (FMA), and the Modified Ashworth Scale (MAS) were used to assess the degree of ankle clonus, ankle passive range of motion, and lower limb motor function of the two groups of patients. Before treatment, there was no statistically significant difference between the control group and the FM group in terms of CSS, PROM, FMA, and MAS of the affected lower limbs (P>0.05). After 3 weeks of treatment, the CSS and MAS of the affected lower limbs in the control group and FM group decreased, while PROM and FMA increased compared to pre-treatment evaluation, with statistically significant differences (P<0.05). Moreover, the FM group showed a statistically significant decrease in CSS and MAS, as well as an increase in PROM and FMA, compared to the control group (P<0.05). Conclusions: Fascial manipulation in addition to conventional therapy can effectively reduce spasticity and ankle clonus in stroke patients in a short time, and improve the passive range of motion of the ankle joint and the function of lower limbs.
... A distinction is made between neuronal and non-neuronal components, and spasticity mainly has a neuronal origin [15]. One of the main factors contributing to the symptom of muscle hypertonia in neurological disorders is the hyperactivity of spinal motor neurons [16]. There is no single definition of spasticity. ...
Stroke is a severe injury of the central nervous system (CNS) and one of the leading causes of long-term disability and mortality. One of the main symptoms of neurological diseases is spasticity. This is defined as a motor condition characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks and resulting in the hyperexcitability of the stretch reflex. Rehabilitation after a stroke is focused on relearning lost skills and regaining independence. Many new methods in neurorehabilitation have been introduced. This review concentrates on the current evidence for extracorporeal shockwave therapy (ESWT) as a noninvasive alternative to treat spasticity. We present the effect of EWST and radial EWST interventions to post-stroke patients with spasticity in the upper limb. Our collected data suggest that different parameters of shockwaves can be used to achieve functional improvementsin the upper limb after a stroke. Our accumulated data imply that ESWT is safe and can be used for pain relief, reduced muscle tension, and an increased range of motion. According to many studies, complications after shockwave treatment are infrequent. Transient complications after shockwave therapy (ESWT) include redness, tingling, pain, and bruising. We reviewed clinical trials that present the possible benefits in upper-limb function after shockwave therapy for post-stroke patients. In this article, we used many database search engines, including PEDro. In the stroke rehabilitation literature, a key methodological problem is the design of double-blind studies, which very often are not feasible.
... spastic hypertonus: [21,25]. Spastic hypertonia is understood to reflect systematic reductions in stretch reflex thresholds [16,24], decreased range of regulation of these stretch reflex thresholds [23,47], as well as altered nonreflex phenomena such as abnormalities in the intrinsic mechanical properties of spastic muscles and altered viscoelastic properties of passive tissues [28,43,49]. Importantly, systematic reduction in stretch reflex threshold could lead to significant increase in stretch reflex excitability [17] and agonist/antagonist coactivation in some regions of the workspace [22,30], which could lead to complex, posture-dependent and potentially time-varying joint impedances in the hemiparetic arm. ...
Background
Muscles in the post-stroke arm commonly demonstrate abnormal reflexes that result in increased position- and velocity-dependent resistance to movement. We sought to develop a reliable way to quantify mechanical consequences of abnormal neuromuscular mechanisms throughout the reachable workspace in the hemiparetic arm post-stroke.
Methods
Survivors of hemiparetic stroke (HS) and neurologically intact (NI) control subjects were instructed to relax as a robotic device repositioned the hand of their hemiparetic arm between several testing locations that sampled the arm's passive range of motion. During transitions, the robot induced motions at either the shoulder or elbow joint at three speeds: very slow (6°/s), medium (30°/s), and fast (90°/s). The robot held the hand at the testing location for at least 20 s after each transition. We recorded and analyzed hand force and electromyographic activations from selected muscles spanning the shoulder and elbow joints during and after transitions.
Results
Hand forces and electromyographic activations were invariantly small at all speeds and all sample times in NI control subjects but varied systematically by transport speed during and shortly after movement in the HS subjects. Velocity-dependent resistance to stretch diminished within 2 s after movement ceased in the hemiparetic arms. Hand forces and EMGs changed very little from 2 s after the movement ended onward, exhibiting dependence on limb posture but no systematic dependence on movement speed or direction. Although each HS subject displayed a unique field of hand forces and EMG responses across the workspace after movement ceased, the magnitude of steady-state hand forces was generally greater near the outer boundaries of the workspace than in the center of the workspace for the HS group but not the NI group.
Conclusions
In the HS group, electromyographic activations exhibited abnormalities consistent with stroke-related decreases in the stretch reflex thresholds. These observations were consistent across repeated testing days. We expect that the approach described here will enable future studies to elucidate stroke's impact on the interaction between the neural mechanisms mediating control of upper extremity posture and movement during goal-directed actions such as reaching and pointing with the arm and hand.
... two consecutive readings were recorded, and the mean score was calculated. the degree of ankle planter flexion was measured as a negative value, and the degree of ankle dorsiflexion was measured as a positive value [19]. 3. the timed 10 meters walk test (10 MWt): comfortable gait speed was assessed using the 10 Meter Walking test (10 MWt). the patient is asked to walk 10 meters on their own throughout two trials for comfortable walking speeds. ...
Purpose:
To evaluate the effectiveness of radial extracorporeal shock wave therapy (r ESWT) as an additional treatment modality for spastic equinus deformity in chronic hemiplegic patients.
Methods:
100 eligible stroke patients with calf muscles spasticity were randomized into 2 groups. Group I: 50 patients exposed to rESWT 1.500 pulses, 0.10 mJ to 0.3mJ/mm2, with a frequency 4 Hz once weekly for one month. Group II: 50 patients exposed to Sham rESWT once weekly for one month. Clinical, electrophysiological & musculoskeletal ultrasound assessments were done for all patients.
Results:
After controlling baseline as covariate, the trend for modified Ashworth scale (MAS), Passive ankle dorsiflexion motion (PADFM), 10 meters walk test (10-MWT), and Ratio of maximum H reflex to maximum M response (H/M ratio) after one & two months was significantly different between the two groups, with improvement of all clinical and electrophysiological parameters in group I.
Conclusion:
ESWT represents a useful non-invasive, additional modality for the reduction of foot spasticity and equinus deformity in stroke patients.
... Spasticity is considered to be the most important cause of functional disability as it leads to increased joint resistance secondary to structural and mechanical changes in skeletal muscle through fibrotic scarring of the connective tissue in poststroke patients. It interrupts the rehabilitation specifically related to function restoration [4,5]. Lower limb spasticity affects gait and limits physical activities and participation in daily living. ...
Objective:
To determine the effects of extracorporeal shock wave therapy (ESWT) on lower limb function, walking, and quality of life in patients with lower limb poststroke spasticity.
Data sources:
A comprehensive and systematic electronic database search of PubMed, Web of Science, ProQuest thesis Dissertation checks, Google Scholar was conducted from January 2010 to March 2022.
Review method:
Initially, the bibliography was screened to identify randomized and nonrandomized controlled trials evaluating the effects of ESWT on lower limb spasticity and functional outcomes in stroke patients. Two reviewers independently screened the title and abstract, full-text articles, extracted data, and assessed the quality of the selected studies. The primary evaluation outcome was spasticity assessed by Modified Ashworth Scale (MAS), and the secondary outcomes were walking performance and quality of life measured on different scales.
Data synthesis:
Out of the total of 483 records, 15 studies (389 participants) were finally found eligible for inclusion. A meta-analysis was performed and beneficial effects of ESWT were observed in the experimental group compared with the control group on spasticity. MAS: Standard mean difference (SMD = 0.626), (95%CI = -0.133, 1.119), (p < 0.01), ROM: (SMD = 0.573), (95%CI = 0.074, 1.072), (p < 0.02). The result for before and after ESWT application on TUG: (SMD = 0.174), (95%CI=-0.151, 0.499), (p = 0.29). The results for walking performance were not significant and inconclusive which may be due to the heterogeneity of the studies included.
Conclusion:
Evidence suggests that ESWT has promising effects in reducing spasticity and improving lower limb motor function. However, uncertainty exists regarding its effectiveness in walking performance.
... Spasticity is a velocity and muscle length-dependent increase in resistance to the externally imposed muscle stretch. 1 It shares similar pathophysiological origins with abnormal synergies, inappropriate muscle activation and anomalous muscle coactivation. 2 Spasticity is mainly a neurogenic phenomenon that results in unopposed excitatory descending inputs to spinal stretch reflex circuits. ...
Introduction/Purpose
To determine the location of the rectus femoris (RF) motor branch nerve, as well as its coordinates with reference to anatomical and ultrasound landmarks.
Methods
Thirty chronic stroke patients with stiff knee gait (SKG) and RF hyperactivity were included. The motor nerve branch to the RF muscle was identified medially to the vertical line from anterior superior iliac spine and the midpoint of the superior margin of the patella (line AP) and vertically to the horizontal line from the femoral pulse and its intersection point with the line AP (line F). The point of the motor branch (M) was located with ultrasound, and nerve depth and subcutaneous tissue thickness (ST) were calculated.
Results
The coordinates of the motor branch to the RF were 2.82 (0.47) cm medially to the line AP and 4.61 (0.83) cm vertically to the line F. Nerve depth and subcutaneous tissue thickness were 2.71 (0.62) cm and 1.12 (0.75) cm, respectively.
Conclusion
The use of specific coordinates may increase clinicians' confidence when performing RF motor nerve block. This could lead to better decision‐making when assessing SKG in chronic stroke patients.
... Upper limb hypertonicity management is an example of a complex area of clinical practice in which occupational therapists regularly work. Hypertonicity is commonly experienced by people with neurological conditions (Burridge et al., 2009;Marciniak, 2011) and is defined as an increased resistance to passive movement (Katz & Rymer, 1989), due to both spasticity and soft tissue stiffness (Sheen & McGuire, 2001). The main therapy aims when addressing hypertonicity are to decrease resistance to movement, increase passive and active range, and, where possible, retrain movement patterns including reaching for, holding, and manipulating items (Copley & Kuipers, 2014) to facilitate participation in daily activities. ...
Introduction : Increasingly, novice occupational therapists are working in private practice. It is important to understand how to build clinical experience in complex practice areas. Upper limb hypertonicity management is a complex practice area requiring advanced workplace training. This study aimed to identify the teaching and learning processes that assist occupational therapists to acquire this expertise.
Methods : Five hospital occupational therapists received 1.5-3 years of apprentice-style training in a specialist hypertonicity clinic. In-depth semi-structured interviews explored their experience. Qualitative Description was used to analyse the data.
Results : Participants found that knowledge needed to be applied to practice and then revisited in a cyclical way to deepen their understanding and build their clinical skills. They benefited from having responsibilities graded and repeated opportunities for hands-on learning of embodied knowledge. Producing comprehensive progress notes and teaching colleagues and students were useful learning tools. Learning with a group of colleagues involved observation of the expert, intensive correction and guidance, and group discussion, reflection and questioning to build expertise.
Conclusion : Workplaces need to intentionally support novice clinicians to gain expertise in complex practice areas using pedagogically sound training techniques. Continuous workplace training is needed to promote expertise in the face of changing healthcare funding policies.
... It is generally believed that the disruption of cortical activity and associated corticospinal drive due to central nervous system (CNS) disorder is often caused by disinhibition of reflex activity, which contributes to spasticity. 4,5 Studies of patients with upper motor neuron syndrome and spasticity indicated that the monosynaptic reflex response to stretch is enhanced, whereas the long-latency (polysynaptic) stretch reflex appears to be reduced in strength. 6 It has also been shown that the lack of an increase in reciprocal inhibition and presynaptic inhibition associated with voluntary movement is responsible for the elicitation of an unwanted stretch reflex activity and co-contraction in patients with spasticity. ...
Objective:
The objective of this study was to identify effective stimulus time by quantifying the inhibitory effects of focal muscle vibration (FMV) on maximal grip strength and muscle activities of the wrist and extrinsic finger flexors.
Methods:
A randomized repeated-measures design was used in this study. A total of 22 healthy volunteers (mean age, 20.9 years) participated. An FMV of 86 Hz was applied to the anterior surface of the distal forearm under the following 3 conditions: no FMV (control), 5-minute FMV, and 10-minute FMV. Maximal grip strength was measured before and after FMV. The muscle activities of the flexor digitorum superficialis, flexor digitorum profundus (FDP), and flexor carpi ulnaris were simultaneously recorded using surface electromyography. Discomfort and complications following FMV were also assessed.
Results:
Compared with the control group, a significant decrease in muscle activity was observed in both the flexor digitorum superficialis and flexor carpi ulnaris after 5 and 10 minutes of FMV. In contrast, there was no significant decrease in the maximal grip strength or FDP muscle activity after either FMV condition. The discomfort was significantly higher immediately after both FMV conditions than in the control group, but it decreased 15 minutes after FMV, indicating no significant difference among the 3 conditions. Redness and/or swelling were observed in 13.6% and 36.3% of the participants after 5 and 10 minutes of FMV, respectively.
Conclusion:
Five-minute FMV to the distal forearm could be a useful therapeutic method with few complications. However, the FMV in this area alone was not sufficient to suppress the muscle activity of the FDP located in the deep layer.
... Second, α-motoneuron (α-MN) hyperexcitability is deemed the abnormal intraspinal change in PSS (44). The reason is probably as follows: augmented sensitivity spindles increase peripheral afferent input to the spinal MN, setting the condition for oversensitivity of the stretch arc (39). ...
With the trend of aging population getting more obvious, stroke has already been a major public health problem worldwide. As a main disabling motor impairment after stroke, spasticity has unexpected negative impacts on the quality of life and social participation in patients. Moreover, it brings heavy economic burden to the family and society. Previous researches indicated that abnormality of neural modulation and muscle property corelates with the pathogenesis of poststroke spasticity (PSS). So far, there still lacks golden standardized treatment regimen for PSS; furthermore, certain potential adverse-events of the mainstream therapy, for example, drug-induced generalized muscle weakness or high risk related surgery somehow decrease patient preference and compliance, which brings challenges to disease treatment and follow-up care. As an essential non-pharmacological therapy, acupuncture has long been used for PSS in China and shows favorable effects on improvements of spastic hypertonia and motor function. Notably, previous studies focused mainly on the research of antispastic acupoints. In comparison, few studies lay special stress on the other significant factor impacting on acupuncture efficacy, that is acupuncture technique. Based on current evidences from the clinic and laboratory, we will discuss certain new insights into acupuncture technique, in particular the antispastic needling technique, for PSS management in light of its potential effects on central modulations as well as peripheral adjustments, and attempt to provide some suggestions for future studies with respect to the intervention timing and course, application of acupuncture techniques, acupoint selection, predictive and aggravating factors of PSS, aiming at optimization of antispastic acupuncture regimen and improvement of quality of life in stroke patients. More innovations including rigorous study design, valid objective assessments for spasticity, and related experimental studies are worthy to be expected in the years ahead.
... Spasticity occurs in terms of the imbalance between inhibitory and excitatory mechanisms due to lateral reticulospinal tract damage [4][5][6][7]. Although the primary cause of spasticity is brain pathways damage, the resulting morphological and biomechanical changes in the affected muscles can exacerbate it over time [8][9][10]. ...
Purpose:
Evaluation the effects of dry needling on sonographic, biomechanical and functional parameters of spastic upper extremity muscles.
Methods:
Twenty-four patients (35-65 years) with spastic hand were randomly allocated into two equal groups: intervention and sham-controlled groups. The treatment protocol was 12-sessions neurorehabilitation for both groups and 4-sessions dry needling or sham-needling for the intervention group and sham-controlled group respectively on wrist and fingers flexor muscles. The outcomes were muscle thickness, spasticity, upper extremity motor function, hand dexterity and reflex torque which were assessed before, after the 12th session, and after one-month follow-up by a blinded assessor.
Results:
The analysis showed that there was a significant reduction in muscle thickness, spasticity and reflex torque and a significant increment in motor function and dexterity in both groups after treatment (p < 0.01). However, these changes were significantly higher in the intervention group (p < 0.01) except for spasticity. Moreover, a significant improvement was seen in all outcomes measured one-month after the end of the treatment in the intervention group (p < 0.01).
Conclusions:
Dry needling plus neurorehabilitation could decrease muscle thickness, spasticity and reflex torque and improve upper-extremity motor performance and dexterity in chronic stroke patients. These changes were lasted one-month after treatment.Trial Registration Number: IRCT20200904048609N1IMPLICATION FOR REHABILITATIONUpper extremity spasticity is one of the stroke consequences which interfere with motor function and dexterity of patient hand in activity of daily livingApplying the dry needling accompanied with neurorehabilitation program in post-stroke patients with muscle spasticity can reduce the muscle thickness, spasticity and reflex torque and improve upper extremity functions.
... slow and fast velocities, are required to unravel joint resistance contributions. Therefore, the MAS can clinically only evaluate spasticity indirectly and cannot distinguish between spasticity and other symptoms as involuntary background activity, shortened soft tissue, contractures and muscle fibrosis [4,12,13]. Furthermore, the MAS has a questionable reliability, especially when applied at the lower limb [11,14]. Hence, the clinical effect of BoNT-A injections on spasticity is poorly understood, while BoNT-A injections are a frequently used clinical intervention for spasticity. ...
Background
Spasticity, i.e. stretch hyperreflexia, increases joint resistance similar to symptoms like hypertonia and contractures. Botulinum neurotoxin-A (BoNT-A) injections are a widely used intervention to reduce spasticity. BoNT-A effects on spasticity are poorly understood, because clinical measures, e.g. modified Ashworth scale (MAS), cannot differentiate between the symptoms affecting joint resistance. This paper distinguishes the contributions of the reflexive and intrinsic pathways to ankle joint hyper-resistance for participants treated with BoNT-A injections. We hypothesized that the overall joint resistance and reflexive contribution decrease 6 weeks after injection, while returning close to baseline after 12 weeks.
Methods
Nine participants with spasticity after spinal cord injury or after stroke were evaluated across three sessions: 0, 6 and 12 weeks after BoNT-A injection in the calf muscles. Evaluation included clinical measures (MAS, Tardieu Scale) and motorized instrumented assessment using the instrumented spasticity test (SPAT) and parallel-cascade (PC) system identification. Assessments included measures for: (1) overall resistance from MAS and fast velocity SPAT; (2) reflexive resistance contribution from Tardieu Scale, difference between fast and slow velocity SPAT and PC reflexive gain; and (3) intrinsic resistance contribution from slow velocity SPAT and PC intrinsic stiffness/damping.
Results
Individually, the hypothesized BoNT-A effect, the combination of a reduced resistance (week 6) and return towards baseline (week 12), was observed in the MAS (5 participants), fast velocity SPAT (2 participants), Tardieu Scale (2 participants), SPAT (1 participant) and reflexive gain (4 participants). On group-level, the hypothesis was only confirmed for the MAS, which showed a significant resistance reduction at week 6. All instrumented measures were strongly correlated when quantifying the same resistance contribution.
Conclusion
At group-level, the expected joint resistance reduction due to BoNT-A injections was only observed in the MAS (overall resistance). This observed reduction could not be attributed to an unambiguous group-level reduction of the reflexive resistance contribution, as no instrumented measure confirmed the hypothesis. Validity of the instrumented measures was supported through a strong association between different assessment methods. Therefore, further quantification of the individual contributions to joint resistance changes using instrumented measures across a large sample size are essential to understand the heterogeneous response to BoNT-A injections.
... spastic hypertonus: Lance, 1980;Li et al., 2021). Spastic hypertonia is understood to reflect systematic reductions in stretch reflex thresholds (Katz and Rymer, 1989;Levin et al., 2000), decreased range of regulation of these stretch reflex thresholds (Levin and Feldman 1994), as well as altered non-reflex phenomena such as abnormalities in the intrinsic mechanical properties of spastic muscles and altered viscoelastic properties of passive tissues (Mirbagheri et al., 2007;Sinkjaer and Magnussen 1994;Zhang et al., 2002). Importantly, systematic reduction in stretch reflex threshold could lead to significant increase in stretch reflex excitability (Knutsson and Owens 2003) and agonist/antagonist coactivity in some regions of the workspace (Levin and Dimov, 1997;Musampa et al., 2007), which could lead to complex, posture-dependent and potentially time-varying joint impedances in the hemiparetic arm. ...
Muscles in the post-stroke arm commonly demonstrate abnormal reflexes that result in increased position- and velocity-dependent resistance to movement. We sought to develop a reliable way to quantify mechanical consequences of abnormal neuromuscular mechanisms throughout the reachable workspace in the hemiparetic arm post-stroke. Survivors of hemiparetic stroke (HS) and neurologically-intact (NI) control subjects were instructed to relax as a robotic device repositioned the hand of their (hemiparetic) arm between several testing locations sampling the arm's passive range of motion. During transitions, the robot induced motions at either the shoulder or elbow joint at speeds ranging from very slow (6 °/s) to fast (90 °/s). The robot held the hand at the testing location for at least 20 seconds after each transition. We recorded and analyzed hand force and electromyographic activities from selected muscles spanning the shoulder and elbow during and after transitions. Hand forces and electromyographic activities were small at all speeds and sample times in NI control subjects, but varied systematically by transport speed during and shortly after movement in the HS subjects. Velocity-dependent resistance to stretch diminished within two seconds after movement ceased in the hemiparetic arms. Hand forces and EMGs changed very little from 2 seconds after the movement ended onward, exhibiting dependence on limb posture but no systematic dependence on movement speed or direction. Although each HS subject displayed a unique field of hand forces and EMG responses across the workspace after movement ceased, the magnitude of steady-state hand forces was generally greater near the outer boundaries of the workspace than in the center of the workspace for the HS group but not the NI group. In the HS group, electromyographic activities exhibited abnormalities consistent with stroke-related decreases in the stretch reflex thresholds post-stroke. These observations were consistent across repeated testing days. Implications of the findings are discussed.
... While difficulties occurring at the joint or muscle level, such as hypertonicity (Katz and Rymer, 1989), spasticity (Opheim et al., 2014), or weakness (Ada et al., 2003;Kamper et al., 2006) certainly contribute to functional deficits, impairment of the coordination activity of multiple joints may have an even more profound effect (Ada et al., 2006). Past studies examining the arm have revealed altered interjoint kinematics in the paretic arm of stroke survivors (Cirstea et al., 2003) and reduced capacity to create the required joint interaction torques (Beer et al., 2000). ...
Despite its importance, abnormal interactions between the proximal and distal upper extremity muscles of stroke survivors and their impact on functional task performance has not been well described, due in part to the complexity of upper extremity tasks. In this pilot study, we elucidated proximal–distal interactions and their functional impact on stroke survivors by quantitatively delineating how hand and arm movements affect each other across different phases of functional task performance, and how these interactions are influenced by stroke. Fourteen subjects, including nine chronic stroke survivors and five neurologically-intact subjects participated in an experiment involving transport and release of cylindrical objects between locations requiring distinct proximal kinematics. Distal kinematics of stroke survivors, particularly hand opening, were significantly affected by the proximal kinematics, as the hand aperture decreased and the duration of hand opening increased at the locations that requires shoulder abduction and elbow extension. Cocontraction of the extrinsic hand muscles of stroke survivors significantly increased at these locations, where an increase in the intermuscular coherence between distal and proximal muscles was observed. Proximal kinematics of stroke survivors was also affected by the finger extension, but the cocontraction of their proximal muscles did not significantly increase, suggesting the changes in the proximal kinematics were made voluntarily. Our results showed significant proximal-to-distal interactions between finger extension and elbow extension/shoulder abduction of stroke survivors exist during their functional movements. Increased cocontraction of the hand muscles due to increased neural couplings between the distal and proximal muscles appears to be the underlying mechanism.
... The muscles were tested over a set of 7 predefined angular velocities(5,30, 60, 90, 120, 150, and 180 degrees per second). During the movement toward dorsiflexion, the APT generated by the spastic ankle plantarflexors while lengthening was measured over the specified range of motion and taken as an index of resistance to passive motion.28 Passive mobilizations started with the low velocities and progressed to the faster ones according to the patient's comfort and tolerability. ...
Objective:
To the best of the authors' knowledge, no data are available about the use of isokinetic resistance training for managing ankle plantarflexor spastic hypertonia in people with multiple sclerosis (MS). The aim of this proof-of-concept study was to explore the feasibility and effects of concentric contractions on spasticity-related resistance to passive motion, strength, and mobility in people who have MS and ankle plantarflexor spasticity.
Methods:
In this pretest/posttest case series, 5 people with MS (mean age = 53.6 [SD = 8.8] years; median Expanded Disability Status Scale score = 5; Modified Ashworth Scale range = 1-4) received 6 weeks of isokinetic resistance training of the spastic plantarflexors. Before and after the intervention, the following outcomes were assessed: average peak torque during passive robotic mobilization, isometric strength, surface electromyography (sEMG) from the spastic muscles, time to complete the 10-Meter Walk Test and the Timed "Up & Go" Test. The standardized effect size was used to test pretest and posttest effects at the individual level. Group-level analyses were also performed.
Results:
Following the training, the average peak torque recorded from the plantarflexors during passive motion at a velocity of 150 degrees per second was found to be decreased by at least 1 SD in all participants but 1, with a significant reduction at the group level of 23.8%. Conversely, no changes in sEMG activity were detected. Group-level analyses revealed that the maximal strength of the trained plantarflexors increased significantly (31.4%). Fast walking speed increased and time to complete the Timed "Up & Go" Test decreased in 4 participants, although not significantly at the group level.
Conclusions:
Isokinetic resistance training proved safe and feasible in people who had MS and ankle plantarflexor spasticity. The observed reductions in resistance to passive motion from the spastic plantarflexors in the absence of sEMG changes might suggest a mechanical rather than a neural effect of the training.
Impact:
Based on these preliminary findings, isokinetic resistance training does not exacerbate hypertonia in people who have MS and ankle plantarflexor spasticity and could be safely used to manage muscle weakness in this population.
... Upper limb motor deficits affect approximately 3 million individuals in the United States alone who have sustained neurological injuries or have conditions such as stroke [1], [2], traumatic brain injury (TBI) [3], [4], spinal cord injury (SCI) or cerebral palsy [5], [6]. These motor impairments can be characterized using positive and negative symptoms [7], [8]. Positive symptoms such as spasticity, a velocity dependent increase in muscle tone, and hypertonicity, stiffness due to increased muscle tone, result in the hand being in a closed fist posture (Fig.1A). ...
Neurological trauma, such as stroke, traumatic brain injury (TBI), spinal cord injury, and cerebral palsy can cause mild to severe upper limb impairments. Hand impairment makes it difficult for individuals to complete activities of daily living, especially bimanual tasks. A robotic hand orthosis or hand exoskeleton can be used to restore partial function of an intact but impaired hand. It is common for upper extremity prostheses and orthoses to use electromyography (EMG) sensing as a method for the user to control their device. However some individuals with an intact but impaired hand may struggle to use a myoelectrically controlled device due to potentially confounding muscle activity. This study was conducted to evaluate the application of conventional EMG control techniques as a robotic orthosis/exoskeleton user input method for individuals with mild to severe hand impairments. Nine impaired subjects and ten healthy subjects were asked to perform repeated contractions of muscles in their forearm and then onset analysis and feature classification were used to determine the accuracy of the employed EMG techniques. The average accuracy for contraction identification across employed EMG techniques was 95.4% ± 4.9 for the healthy subjects and 73.9% ± 13.1 for the impaired subjects with a range of 47.0% ± 19.1 - 91.6% ± 8.5. These preliminary results suggest that the conventional EMG control technologies employed in this paper may be difficult for some impaired individuals to use due to their unreliable muscle control.
... In unhealthy muscle, the normal neuromuscular pathway is disrupted resulting in muscle function abnormalities and pain. The hyperexcitability of neurons produces muscle hypertonicity, which causes the muscle to constantly contract, resulting in pain and, over time, tetany [64] . FES will disturb this neural hyperexcitability, returning the muscle to balanced contraction and relaxation phases, therefore reducing pain [65] . ...
When diagnosing neuromuscular injury and pain, the use of biomechanical evaluations to assess the mechanics of movement patterns has been useful in the human population. Functional electrical stimulation (FES) is a technology which can create action potentials to produce musculoskeletal movement that is almost indistinguishable from the voluntary kinematics produced by the nervous system. To create controlled and precise musculoskeletal movements in humans and in horses, FES has been shown to be effective. In humans, the kinematic information obtained from FES data has been utilized to direct further diagnostics, and/or to assist in the development of specific treatment protocols. In addition, since FES creates dynamic movement while in a static position, the ability to isolate the regions of dysfunction improves without the confounding factors of over the ground movement and other artifacts caused by environmental stimuli. This paper explores the transfer of the use of FES in human diagnostics to clinical use in horses. Three equine case studies discuss how FES was employed as a tool in the diagnosis and treatment of equine musculoskeletal and neuromuscular control disorders.
... Stroke is one of the leading causes of long-term disability in adults (Crichton et al., 2016). Possible sequela associated with upper motor neuron lesions following stroke include muscle weakness, fatigability and spasticity, all of which contribute to impaired motor function (Dietz and Sinkjaer, 2007;Katz and Rymer, 1989). Alterations in muscle structure and composition are also evident after stroke (Hafer-Macko et al., 2008;Lieber et al., 2004) with increased passive muscle stiffness and tension at rest (Lieber et al., 2004). ...
Background
This study aimed to investigate the structural, morphological and passive mechanical properties of the medial gastrocnemius muscle among ambulating chronic stroke survivors using a computational model previously established in healthy individuals without stroke.
Methods
Individuals with chronic stroke (n = 14, age = 63.4 ± 6.0 years) and healthy controls (n = 15, age = 59.6 ± 8.4 years) participated in the study. The mechanical properties of the medial gastrocnemius were measured during continuous passive ankle motion using ultrasound elastography and a corresponding muscle mechanical property-angle curve was estimated where slack angle and elasticity were determined. Muscle thickness, fascicle length, pennation angle, and echo intensity were also assessed using B-mode ultrasound.
Findings
No significant differences in slack angle (paretic: −16.2° ± 6.13°, non-paretic: −16.93° ± 6.80°, p = 0.82), or slack elasticity (paretic: 4.36 ± 1.94 kPa, non-paretic: 4.54 ± 1.24 kPa, p = 0.64) were found between sides or groups. Lower muscle pennation angle (paretic: 13.6 ± 2.9°, non-paretic: 15.9 ± 2.0°, p = 0.019) and higher echo intensity (paretic: 80.5 ± 13.6, non-paretic: 63.4 ± 17.1, p = 0.003) were observed for paretic muscles. No significant between-sides differences were found for muscle thickness (paretic: 1.5 ± 0.3 cm, non-paretic: 1.6 ± 0.2 cm, p = 0.255) or fascicle length (paretic: 6.6 ± 1.9 cm, non-paretic: 7.1 ± 2.2 cm, p = 0.216). Significant between-groups difference was also observed for fascicle length [non-dominant side (control): 6.2 ± 0.8 cm, paretic side (stroke): 6.6 ± 1.9 cm, p = 0.017].
Interpretation
Although muscle mechanical properties increased exponentially over the slack ankle, measures between paretic and non-paretic sides were similar in ambulating participants with chronic stroke. Side-to-side differences in structural and morphological measures suggest the impact of stroke was relatively more pronounced for these muscle parameters than for passive mechanical properties.
... S PASTICITY is a motor disorder induced by the hyperexcitability of tonic stretch reflexes [1], resulting in a velocity-dependent increase in muscle tone with exaggerated tendon jerk, as a common clinical manifestation of upper motor neuron syndrome following central nervous system injuries [2]- [4]. The pathophysiology of spasticity leads to movement disorders and functional disability [5], [6], and therapeutic techniques (e.g. physical and surgical treatments) are currently available to control the disease progression [7]. ...
Spasticity is a common disabling complication caused by the upper motor neurons dysfunction following neurological diseases such as stroke. Currently, the assessment of the spastic hypertonia triggered by stretch reflexes is manually performed by clinicians using perception-based clinical scales, however, their reliability is still questionable due to the inter-rater and intra-rater variability. In order to objectively quantify the complex spasticity phenomenon in post-stroke patients, this study proposed a multi-layer assessment system based on a novel measurement device. The exoskeletal device was developed to synchronously record the kinematic, biomechanical and electrophysiological information in sixteen spastic patients and ten age-matched healthy subjects, while the spastic limb was stretched at low, moderate and high velocities. The mechanical impedance of the elbow joint was identified using a modified genetic algorithm to quantify the alterations in viscoelastic properties underlying pathological resistance. Simultaneously, the time-frequency features were extracted from the surface electromyography (sEMG) signals to reveal the neurophysiological mechanisms of the spastic muscles. By concatenating these single-layer decisions, a support vector regression (SVR)-based fusion model was developed to generate a more comprehensive quantification of spasticity severity. Experimental results demonstrated that the stiffness and damping components of the spastic arm significantly deviated from the nonspastic baseline, and strong correlations were observed between the proposed spasticity assessment and the severity level measured by clinical scales (
), as well as the tonic stretch reflex threshold (TSRT) value (
). These promising results suggest that the proposed assessment system holds great potential to support the clinical diagnosis of motor abnormalities in spastic patients, and ultimately enables optimal adjustment of treatment protocols.
... Patients showing limited upper limb motor recovery are likely to develop increased resistance to passive wrist extension, i.e. wrist hyper-resistance, in weeks to months post stroke [6,7]. This hyper-resistance of the wrist joint is hypothesized to originate from a complex interaction between impaired neuromuscular activation and altered tissue properties of the muscles spanning the joint [8,9]. Impaired neuromuscular activation includes spasticity, defined as velocity-dependent stretch hyperreflexia [10], and involuntary background activation [11]. ...
Patients with poor upper limb motor recovery after stroke are likely to develop increased resistance to passive wrist extension, i.e., wrist hyper-resistance. Quantification of the underlying neural and non-neural elastic components is of clinical interest. This cross-sectional study compared two methods: a commercially available device (NeuroFlexor®) with an experimental EMG-based device (Wristalyzer) in 43 patients with chronic stroke. Spearman's rank correlation coefficients (r) between components, modified Ashworth scale (MAS) and range of passive wrist extension (PRoM) were calculated with 95% confidence intervals. Neural as well as elastic components assessed by both devices were associated (r=0.61, 95%CI:0.38-0.77 and r=0.53, 95%CI:0.28-0.72, respectively). The neural component assessed by the NeuroFlexor® associated with the elastic components of NeuroFlexor® (r=0.46, 95%CI:0.18-0.67) and Wristalyzer (r=0.36, 95%CI:0.06-0.59). The neural component assessed by the Wristalyzer was not associated with the elastic components of both devices. Neural and elastic components of both devices associated similarly with the MAS (r=0.58, 95%CI:0.34-0.75 vs. 0.49, 95%CI:0.22-0.69 and r=0.51, 95%CI:0.25-0.70 vs. 0.30, 95%CI:0.00-0.55); elastic components associated with PRoM (r=-0.44, 95%CI:-0.65- -0.16 vs. -0.74, 95%CI:-0.85- -0.57 for NeuroFlexor® and Wristalyzer respectively). Results demonstrate that both methods perform similarly regarding the quantification of neural and elastic wrist hyper-resistance components and have an added value when compared to clinical assessment with the MAS alone. The added value of EMG in the discrimination between neural and non-neural components requires further investigation.
... We postulated that the MAS measured by the passive stretch test may be inconsistent to that during standing or walking 56 . Static spasticity can originate from hyperactive reflexes, and/ or to stiffiness in muscles or connective tissues 57 . Conversely, dynamic spasticity may tend to increase coupling between muscle-tendon stretch velocity (or change of tissue length) and nonreflex muscular contraction 58 . ...
Spasticity measured by manual tests, such as modified Ashworth scale (MAS), may not sufficiently reflect mobility function in stroke survivors. This study aims to identify additional ambulatory information provided by the pendulum test. Clinical assessments including Brünnstrom recovery stage, manual muscle test, MAS, Tinetti test (TT), Timed up and go test, 10-m walk test (10-MWT), and Barthel index were applied to 40 ambulant chronic stroke patients. The pendular parameters, first swing excursion (FSE) and relaxation index (RI), were extracted by an electrogoniometer. The correlations among these variables were analyzed by the Spearman and Pearson partial correlation tests. After controlling the factor of motor recovery (Brünnstrom recovery stage), the MAS of paretic knee extensor was negatively correlated with the gait score of TT (r = − 0.355, p = 0.027), while the FSE revealed positive correlations to the balance score of TT (r = 0.378, p = 0.018). RI were associated with the comfortable speed of 10-MWT (r = 0.367, p = 0.022). These results suggest a decrease of knee extensor spasticity links to a better gait and balance in chronic stroke patients. The pendular parameters can provide additional ambulatory information, as complementary to the MAS. The pendulum test can be a potential tool for patient selection and outcome assessment after spasticity treatments in chronic stroke population.
Background: Gait and balance alterations in post-stroke patients are one of the most disabling symptoms that can persist in chronic stages of the disease. In this context, rehabilitation has the fundamental role of promoting functional recovery, mitigating gait and balance deficits, and preventing falling risk. Robotic end-effector devices, like the G-EO system (e.g., G-EO system, Reha Technology, Olten, Switzerland), can be a useful device to promote gait recovery in patients with chronic stroke. Materials and Methods: Twelve chronic stroke patients were enrolled and evaluated at baseline (T0) and at post-treatment (T1). These patients received forty sessions of robotic gait training (RGT) with the G-EO system (experimental group, EG), for eight weeks consecutively, in addition to standard rehabilitation therapy. The data of these subjects were compared with those coming from a sample of twelve individuals (control group, CG) matched for clinical and demographic features who underwent the same amount of conventional gait training (CGT), in addition to standard rehabilitation therapy. Results: All patients completed the trial, and none reported any side effects either during or following the training. The EG showed significant improvements in balance (p = 0.012) and gait (p = 0.004) functions measured with the Tinetti Scale (TS) after RGT. Both groups (EG and CG) showed significant improvement in functional independence (FIM, p < 0.001). The Fugl-Meyer Assessment—Lower Extremity (FMA-LE) showed significant improvements in motor function (p = 0.001, p = 0.031) and passive range of motion (p = 0.031) in EG. In EG, gait and balance improvements were influenced by session, age, gender, time since injury (TSI), cadence, and velocity (p < 0.05), while CG showed fewer significant effects, mainly for age, TSI, and session. EG showed significantly greater improvements than CG in balance (p = 0.003) and gait (p = 0.05) based on the TS. Conclusions: RGT with end-effectors, like the G-EO system, can be a valuable complementary treatment in neurorehabilitation, even for chronic stroke patients. Our findings suggest that RGT may improve gait, balance, and lower limb motor functions, enhancing motor control and coordination.
The neural processes underlying gait retraining interventions that combine stepping practice with electrical stimulation are poorly understood. The purpose of this study was to compare acute changes in corticomotor excitability measured by motor evoked potential (MEP) amplitude, monosynaptic stretch reflex excitability measured by H/M ratio, and propulsive force generation during gait measured by anterior ground reaction forces (AGRF), induced by 30-minutes of fast walking (Fast) and 30-minutes of fast walking with functional electrical stimulation of the ankle plantarflexors and dorsiflexors (FastFES) in 14 able-bodied young adults. Our results showed that FastFES, but not Fast elicited a significant acute decrease in tibialis anterior MEP amplitude (p = .01). Furthermore, the practice-induced acute decrease in tibialis anterior MEP amplitudes was significantly larger for FastFES than Fast (p = .04). FastFES also elicited a statistically significant increase in the AGRF in the tested limb (p = .01), which was significantly larger than the change induced by Fast (p = .04). Additionally, baseline soleus MEP amplitude was positively correlated with within-session change in AGRF (p = .04, r² = 0.16). Acute decrease in tibialis anterior MEP amplitude for the FastFES condition relative to the Fast condition may be caused by fatigue, while the greater increase in AGRF for the FastFES condition signify that stepping practice facilitated alterations of gait patterns. More research is needed to confirm neural mechanisms and investigate the acute as well as long-term effects of Fast and FastFES on clinical populations.
Spasticity is a common motor symptom that disrupt muscle contraction and hence movements. Proper management of spasticity requires identification of its origins and reasoning of the therapeutic plans. Challenges arise because spasticity might originate from elevated activity in both the cortical and sub-cortical pathways. No existing models (animal or computational) could cover all possibilities leading to spasticity, especially the peripheral causes such as hyperreflexia. To bridge this gap, this work develops a novel computational, spike-based neuromorphic model of spasticity, named NEUSPA. Rather than relying solely on a monosynaptic spinal loop comprising alpha motoneurons, sensory afferents, synapses, skeletal muscles, and muscle spindles, the NEUSPA model introduces two additional inputs: additive (ADD) and multiplicative (MUL). These inputs generate velocity-dependent EMG responses. The effectiveness of the NEUSPA model is validated using classic experiments from the literature and data collected from two post-stroke patients with affected upper-limb movements. The model is also applied to simulate two real-world scenarios that patients may encounter. Simulation results suggest that hyperreflexia due to extra inputs was sufficient to produce spastic EMG responses. However, EMG onsets were more sensitive to ADD inputs (slope = 0.628, p < 0.0001, r² = 0.96) compared to MUL inputs (slope = 0.471, p < 0.0001, r² = 0.92). Additionally, simulation of finger-pressing on a deformable object indicated that spasticity could increase the duration from 1.03s to 1.20s compared to a non-impaired condition. These results demonstrate that NEUSPA effectively synthesizes abnormal physiological data, facilitating decision-making and machine learning in neurorehabilitation.
Background
Previous studies showed that repetitive transcranial magnetic stimulation (rTMS) reduces spasticity after stroke. However, clinical assessments like the modified Ashworth scale, cannot discriminate stretch reflex-mediated stiffness (spasticity) from passive stiffness components of resistance to muscle stretch. The mechanisms through which rTMS might influence spasticity are also not understood.
Methods
We measured the effects of contralesional motor cortex 1 Hz rTMS (1200 pulses + 50 min physiotherapy: 3×/week, for 4–6 weeks) on spasticity of the wrist flexor muscles in 54 chronic stroke patients using a hand-held dynamometer for objective quantification of the stretch reflex response. In addition, we measured the excitability of three spinal mechanisms thought to be related to post-stroke spasticity: post-activation depression, presynaptic inhibition and reciprocal inhibition before and after the intervention. Effects on motor impairment and function were also assessed using standardized stroke-specific clinical scales.
Results
The stretch reflex-mediated torque in the wrist flexors was significantly reduced after the intervention, while no change was detected in the passive stiffness. Additionally, there was a significant improvement in the clinical tests of motor impairment and function. There were no significant changes in the excitability of any of the measured spinal mechanisms.
Conclusions
We demonstrated that contralesional motor cortex 1 Hz rTMS and physiotherapy can reduce the stretch reflex-mediated component of resistance to muscle stretch without affecting passive stiffness in chronic stroke. The specific physiological mechanisms driving this spasticity reduction remain unresolved, as no changes were observed in the excitability of the investigated spinal mechanisms.
Spasticity is a common complication of spinal cord injuries, affecting up to 80% of people with these injuries. It is a type of muscle tone abnormality that is characterized by involuntary muscle contractions and an increase in muscle tone or stiffness. The severity of spasticity can vary depending on the level and severity of the injury, and it can significantly impact an individual’s quality of life, as well as their ability to carry out daily activities. In this chapter, the author provides an overview of the pathophysiology of spasticity, including how damage to the spinal cord can lead to changes in the way that muscles are controlled. They also discuss the clinical definition of spasticity, which is based on several criteria, including the velocity-dependent resistance to passive joint movement, hyperactive muscle stretch reflex, and clonus. The chapter highlights the dynamic nature of spasticity, which can change over time and in response to various stimuli. As a result, managing spasticity can be challenging, and the author discusses several approaches to treatment, including medications, physical therapy, and assistive technologies. In addition to spasticity, the chapter also covers the related issue of contractures, which are a consequence of spasticity and can lead to stiffness and limited range of motion in joints. The author describes the causes and risk factors for contractures and provides recommendations for their prevention and management. Overall, this chapter provides a comprehensive overview of spasticity and contractures in spinal cord injuries, including their definition, pathophysiology, and management. It highlights the importance of careful monitoring and individualized treatment to improve the quality of life of people with these injuries.
Spasticity is a motor disorder integrated in the upper motor neuron syndrome resulting from central nerve diseases such as stroke. The multifactorial nature of spasticity manifestations leads to the inter-rater and intrarater reliability of clinical assessment, hence, the objective severity quantification of the spastic hypertonia has attracted significant attention in the context of post-stroke rehabilitation. Here, we developed a novel assessment system to reliably identify the exaggerated muscle tone and quantitatively estimate the symptom severity in patients with upper limb spasticity. Twenty subjects with post-stroke spasticity (53.0 ± 13.9 years old) and ten age-matched healthy subjects performed the passive stretch movements under the single-task and dual-task protocols while wearing an exoskeletal measurement device developed by us. A preliminary identification layer was designed to discriminate the pathological electrophysiological outputs of the upper extremity muscles by using the long short-term memory (LSTM) networks. In the next layer, the severity quantification models can be triggered in parallel, aiming at evaluating the neural and non-neural level pathologies underlying the spastic resistance manually percepted by clinicians, where the muscle activation/co-activation features, kinematic departure, and biomechanical characteristics were considered to improve the clinical relevance. Based on these single-level decisions, the third layer was constructed as an integrated model to yield a more comprehensive quantification of the symptom severity. The experimental validation of the proposed system demonstrated good reliability in discriminating the spastic hypertonia from the normal muscle tone, as well as strong agreement of the quantitative severity estimations with the commonly accepted clinical scales for the neural level
, non-neural level
, and integrated level
. In conclusion, the proposed assessment system holds great promise to provide clinicians with an easy-to-use tool as suitable support for spasticity diagnosis, disease monitoring, and treatment adjustment.
Background:
The Hypertonicity Intervention Planning Model (HIPM) is a decision-making aid which guides clinical reasoning in individualizing upper limb (UL) neurorehabilitation.
Aim:
To examine the HIPM's clinical utility across cultures, using therapists' perceptions of its usefulness and challenges when applied in clinical practice.
Methods:
Interpretive description methodology guided qualitative data collection and analysis because it produces clinically practical applications. Forty-four occupational therapists working in Australia or Singapore participated. Three group discussions were conducted using a modified nominal group technique.
Results:
Three themes were: (1) The HIPM guides systematic clinical decision-making for assessment, goal-setting, and intervention; (2) Utility was influenced by systemic or organizational supports and barriers including availability of time, resources, and funding; organizational readiness to change; multidisciplinary and transorganizational collaboration; (3) Therapists' skills and confidence to apply the HIPM, and openness to changing practice, influenced utility.
Conclusions:
Therapists strongly support HIPM use for structuring and communicating clinical reasoning in UL neurorehabilitation. However, organizational support is key to optimizing clinical utility. Incorporating decision-making aids into documentation and referral processes may strengthen multidisciplinary and transorganizational teamwork, enhancing clinical use. Different training tiers to suit therapist experience levels, refresher courses, and supplementary resources may improve therapists' skills and confidence, thereby boosting utility.
After a stroke or spinal cord injury (SCI), there exists an inherent individual capacity for recovery of function that depends on factors such as location and severity of central nervous system (CNS) damage. This capacity can be determined early after the incident by clinical, electrophysiological, and imaging examinations. These measures can also be used as prognostic factors and, consequently, for an early selection of appropriate rehabilitation procedures. Recovery of function after a stroke mainly depends on the tract damaged and the amount of damage, e.g., recovery of hand/finger function is particularly poor after extensive lesioning of the corticospinal tract. In cervical SCI, the combination of peripheral and central nervous system damage limits recovery. As the recovery of function usually remains incomplete, an integral part of rehabilitation should be directed to compensate for the remaining motor deficit by customized assistive devices that promote independence in daily life activities. The capacity for the recovery of function can be exploited by a repetitive execution of functional movements, physically supported as far as required. This approach encourages participation by the patient and promotes appropriate proprioceptive input from limb muscles, tendons, skin, and joints under physiological movement conditions. The consequence of this knowledge is that robotic assistance has to be adapted to the actual condition and requirements of the individual patient. Furthermore, intensive training (i.e., a high number of movement repetitions and long training duration) can lead to an additional gain in function compared to low-dose conventional training. However, this gain is small compared to the spontaneous recovery of function and is often transient, due to the fact that patients will not regularly use these functions in daily life, thereby maintaining them. Finally, other promising adjuvant approaches could contribute to improving motor function in the future, such as epidural or deep brain stimulation as well as CNS repair. However, they are still in an early clinical or in a translational stage.
Spasticity is a disabling problem for many adults and children with a variety of neurological disorders such as multiple sclerosis, stroke, cerebral palsy and traumatic brain injury. A practical guide for clinicians involved in the management of spasticity, this book covers all aspects of upper motor neurone syndrome from basic neurophysiology and measurement techniques to practical therapy and the use of orthoses. Surgical techniques are also covered, as well as the particular problems of management of spasticity in childhood. In the second edition of this key text, all chapters have been thoroughly updated, with additional coverage of new techniques and new drugs and therapies, whilst continuing the format that has made the first edition the core text in its field. This guide will be invaluable to physicians, physiotherapists, surgeons, orthotists, clinical engineers and health professionals.
This chapter discusses the various oral medications used and studied for the treatment of spasticity. The more common oral medications currently used are baclofen and benzodiazepines like diazepam (GABA agonists), tizanidine (alpha 2 receptor agonist), and dantrolene sodium (peripherally acting, decreases calcium release in the skeletal muscle). Other medications control spasticity by blocking voltage-gated ion channels. Sodium channel blockers that have been studied for spasticity management are primarily anti-epileptic drugs (phenytoin, oxcarbazepine, levetiracetam, and lamotrigine). Calcium channel blockers include gabapentin and pregabalin. Tolperisone acts by blocking both the sodium and calcium channels. Other medications used in the management of spasticity and/or spasms, whose mechanism of action is not well defined, include cannabis, cyclobenzaprine, orphenadrine, and mexiletine. Tiagabine (a GABA-mimetic agent), 4-aminopyridine (a potassium channel blocking agent), and cyproheptadine (a serotonin/alpha receptor antagonist) have also been studied for the treatment of spasticity.KeywordsSpasticityOral anti-spasticity medicationsGABA agonistsAlpha-2 agonistSodium channel blockersCalcium channel blockersCannabis
The syndrome of spastic paresis consists of two superimposed disorders: a neural disorder and a non-neural or muscle disorder. Here we describe a clinical five-step assessment, based on the pathophysiology of events that follow lesions to central motor pathways, to assess the neural and non-neural components. Step 1 assesses the functional spastic movement disorder in the upper and lower limbs (using the Modified Frenchay Scale for the upper limb, and ambulation speed for the lower limb). Steps 2–4 evaluate the various forms of muscle resistance encountered during passive and active movements. The Tardieu Scale is used to evaluate passive movement from a position of minimal stretch of the muscle group to completion of full range of motion of the joint. Step 5 assesses rapid alternating movements to determine fatiguability. Several coefficients of impairment can be calculated based on the five-step assessment to assist in developing comprehensive treatment strategies.KeywordsPathophysiologySpastic paresisClinical assessmentStrokeQuantification
Spasticity can cause serious problems in the activity and participation of people with spinal cord injuries. It can also be a significant challenge for rehabilitation. Spasticity is usually defined as a velocity-dependent increase in the tonic stretch reflex (muscle tone) with exaggerated tendon jerks, clonus, and spasms, resulting from the hyperexcitability of the stretch reflex. Current management approaches, including new drugs and technologies, can provide significant benefits for people with spinal cord injuries. This chapter aims to provide an overview of spasticity in spinal cord injuries, including definition, pathophysiology, and management.KeywordsSpasticityUpper motor neuron lesionSpinal cord injuries
This study investigated changes of gait pattern induced by a 4-week robot-assisted gait training (RAGT) in twelve ambulatory spastic diparesis children with cerebral palsy (CP) aged 10.4+/-3.2 years old by using computerized gait analysis (CGA). Pre-post intervention CGA data of children with CP was contrasted to the normative data of typically developing children by using cross-correlation and statistically evaluated by a Wilcoxon test. Significant pre-post intervention changes (p<0.01) include: decreased muscle activity of biceps femoris, rectus femoris, and tibialis anterior; a decrease in range of internal hip joint rotation, higher cadence, step length, and increased stride time. This study suggests that RAGT can be used in muscle reeducation and improved hip joint motion range in ambulatory children with CP.
Background: Shoulder disorders are still one of the major health problems in clinical practice, and shoulder pain is
the third most common type of musculoskeletal pain after spinal and knee pain. The shoulder pain and disability
index (SPADI) is a self-report questionnaire developed to measure the pain and disability associated with shoulder
pathology. SPADI was developed by Roach et al, and has been found to be the quickest (within five minutes) and
easiest to complete.
Method: The study was carried out in three phases: the first was translation into Guajarati and cultural adaptation
of the questionnaire; the second phase was pilot study to assess comprehensibility of the pre final version; third was
the validity and reliability study of the final version of the questionnaire. Total 100 patients aged between 30 to 60
years were included in the study. Then they were asked to fill the SPADI questionnaire twice with the time interval of
24 hours in order to assess test retest reliability of the questionnaire. The test retest reliability and internal
consistency were measured.
Result: The obtained data of 100 patients were analyzed by SPSS version 20. Reliability estimated by internal
consistency using Cronbach’s alpha (0.99) and test retest reliability estimated by interclass correlation coefficient
(0.99) (spearmen’s correlation coefficient) suggest excellent test retest reliability and high correlations between
baseline and retest questionnaires of Guajarati version of shoulder pain and disability index (SPADI).
Conclusion: Gujarati version of shoulder pain and disability index (SPADI) is valid and reliable tool for assessment
of functional status among Guajarati speaking Indian population with shoulder pain.
KEYWORDS: Shoulder pain and disability index (SPADI); Shoulder pain; Test retest reliability; Validity; Gujarati
version; Interclass correlation coefficient (ICC).
In post-stroke hemiparesis, neural impairment alters muscle control, causing abnormal movement and posture in the affected limbs. A decrease in voluntary use of the paretic arm and flexed posture during rest also induce secondary tissue transformation in the upper limb muscles. To obtain a specific, accurate, and reproducible marker of the current biological status of muscles, we collected visible (VIS) and short-wave Infrared (SWIR) reflectance spectra in vivo using a portable spectroradiometer (350–2500 nm), which provided the spectral fingerprints of the elbow flexors and extensors. We compared the spectra for the affected and unaffected sides in 23 patients with post-stroke hemiparesis (25–87 years, 8 women) and eight healthy controls (33–87 years, 5 women). In eight patients, spectra were collected before and after botulinum toxin injection. Spectra underwent off-line preprocessing, principal component analysis, and partial least-squares discriminant analysis. Spectral fingerprints discriminated the muscle (biceps vs. triceps), neurological condition (normal vs. affected vs. unaffected), and effect of botulinum toxin treatment (before vs. 30 to 40 days vs. 110 to 120 days after injection). VIS-SWIR spectroscopy proved valuable for non-invasive assessment of optical properties in muscles, enabled more comprehensive evaluation of hemiparetic muscles, and provided optimal monitoring of the effectiveness of medication.
In a preliminary study a group of hemiplegic patients have been assessed for return of arm function for periods up to 64 weeks after stroke. The assessment procedure employs a few simple and easily performed tests which take into account principles of the central nervous control of movement. The tests are highly repeatable and can be carried out by staff untrained in medicine or any form of physical therapy. Patients have been divided into two groups on the basis of the scores obtained in the tests at 16 weeks after stroke. The group scoring 80% or more are very likely subsequently to recover useful function of the arm and hand. The group of patients scoring less than 80% at 16 weeks after stroke are likely subsequently to recover limited arm movements and little hand movement. The preliminary results would suggest that the tasks provide a guide to prognosis and an indiction of the most suitable type of general physical therapy.
A number of approaches have been advocated for the management of spasticity. The purpose of this review is to discuss the experimental studies that investigated the underlying mechanisms, as well as the clinical benefits, of three of these techniques: local cooling, vibration therapy, and electrical stimulation. First, prolonged local cooling of the spastic muscle has been found to relieve spasticity by reducing the hyperexcitability of tendon reflexes and ankle clonus. Of clinical significance is the long-term functional improvement demonstrated by an increase in range of movement and voluntary power of the antagonist. Second, low amplitude, high-frequency vibration of the paralytic antagonist of a spastic muscle is believed to reduce the hypertonus of the spastic muscle through reciprocal inhibition, while facilitating movement of the paralytic muscle through generation of the tonic vibration reflex conducted via spindle afferents. However, the long-term improvement in neuromuscular function has so far been found to be an increase in the active range of movement, without a significant increase in the voluntary power of either vibrated or nonvibrated muscles. Third, surface electrical stimulation of peripheral nerves, and of spastic or paralytic muscles, has been found to suppress spasticity. Of importance to the therapist is the long period of reduced spasticity observed after the stimulation.
This paper reviews the possible anatomical and physiological factors determining spasticity. All of the major supraspinal motor centres are involved in regulating muscle tone and segmental reflex excitability. Disruption of their output to the spinal cord leads to abnormalities in muscle tone. Characterization of the disorders of segmental reflex function in spasticity is, as yet, incomplete. A number of hypotheses which have been advanced to explain spasticity are discussed with reference to the available evidence. The bulk of experimental evidence does not support the hypothesis of gamma hyperactivity as the main cause of spasticity. Nonreflexogenic alpha hyperexcitability is also unlikely to contribute greatly to spasticity. Switching of reflex pathways, however, appears to determine the distribution of hypertonia and hyperreflexia. Other hypotheses of synaptic plasticity and defective presynaptic inhibitory mechanisms have received some indirect support. Recommendations for future research are made.
This paper is concerned entirely with problems involving the clinical estimation of rigidity, specifically in patients who have Parkinson's disease or are suspected of having this condition. By clinical estimation is meant the various manipulations and techniques used by the neurologist in the standard neurological examination and some speCial tests particularly designated to measure rigidity. It does not concern any of the techniques involving apparatus for measuring resistance of muscles passively or any of the computer or electronic equipment reported in other sections of this volume for the quantitative measurement of this state.
A method is described for quantitating spasticity in the forearm or lower leg. The limb is carried through passive, linear motion at varying angular velocities. At high velocities forceful spasms develop opposing the direction of rotation. The degree of muscular reaction is plotted as torques with characteristic amplitudes and time durations, and the torque magnitude integrated into a meaningful work measurement. Spasticity is defined as the work output in response to angular velocity input per 100 degree cycle (back and forth), of passive motion. A spasticity index obtained from the total work value at varying velocities may be used as a measure o f drug response, and is reportable' in fundamental physical units. A wide range of antispastie agents has been tested and many have proved effective for short periods when administered intravenously. Diazepam, given orally in one case, effectively reduced spasticity for 5 weeks.
Instrumentation and methods are described for measuring and recording in an eight-channel system a variety of muscular and electromyographic variables that are regarded as appropriate to the objective study o f spasticity and other related neurophysiologic responses. These variables include resistive forces developed in extensor and flexor muscles elicited by passive stretching through the full are o f motion, tensive forces developed in response to tendon tap, in eliciting deep muscle myotatic reflexes, and angle o f swing in unrestricted responses of the same type. Correlated electromyographic potentials are recorded in both extensor and flexor muscles concurrently with the muscular resistive forces and the angle of motion. A case study is presented to illustrate the sensitivity and consistency o f the procedures in detecting effects from spasmolytic medication in altering the responses of a patient with clinically evident spasticity. Conclusions are particularized for the individual case presented. Numerous problems, including statistical methods and experimental designs, are being studied with a view toward planning systematic investigation of medication effects in patients with clinical manifestations of hypertonicity and hyperreflexia.
With a device to measure the resistance offered by the middle finger to being driven externally by a D.C. servo motor running at a constant speed, the rheologic properties inherent in muscle (elasticity, viscosity, plasticity) are studied as a basis o f muscle tone, independently of neurally mediated "tonus" or "postural contraction." Provision is made for electromyographic monitoring with intramuscular electrodes and the strain gage output is recorded by an oscillograph and an oscilloscope. The resulting record appears as a Lissajous pattern on the oscilloscope with the torque (Kg.-cm.) recorded on the vertical axis, and displacement (degrees) on the horizontal axis. By this device the stiffness o f the finger is recorded in terms of torque resisting sinusoidal position change. Such data maybe used to study effects of peripheral anesthesia and tension after voluntary contraction. It may also be offered as a useful tool for evaluating the effects o f drugs on spasticity and rigidity.
The essential message of this brief review is that spasticity is not a clinical entity but a variety of entities, each produced by differing types of disturbance in the complex of neurological systems that continuously modulate motor unit activity in the striated muscles. Every spastic patient is different from every other spastic patient, and therefore any rigid categorisation of physiotherapeutic regimes intended to be applied to the spastic patient' is based on a naive view of a highly complex situation. Enough data are now available to provide a basis for a more flexible approach to the therapeutic problems presented to physiotherapists by their spastic patients.
Spasticity, seen so frequently in clinical situations, presents motor signs resembling those produced experimentally by transecting the brain stem of a cat at the intercollicular level. This paper reviews experimental results which elucidate the roles of different brain regions in the genesis of classical decerebrate rigidity and demonstrate the function of the gamma motor system in the maintenance of the rigidity. Interruption of the gamma-spindle loop of a muscle (i.e. interrupting the monosynaptic reflex arc subserving the stretch reflexes) abolishes rigidity in that muscle. This reflex-mediated gamma support of decrebrate rigidity is also a prominent feature of clinical spasticity, making classical decerebrate rigidity a useful model for studying the neural mechanisms underlying spasticity. Not all rididities, however, are gamma dependent. Those rigidities surviving dorsal root rhizotomy are called alpha rigidity. Alpha rigidity results when a brain lesion disrupts descending systems which normally exert a net inhibitory effect upon alpha motoneurons.
The descending facilitatory and inhibitory influences coming to the cord from the brain modulate spinal reflexive activity, thereby allowing the normally functioning nervous system to control purposeful movements in a smooth and efficient manner. Lesions which alter descending paths are reflected at the motoneuron level, either directly or through internuncial spinal cord cells. Interference with descending facilitatory influences may result in an inability to elicit reflex activity, muscular flaccidity and hypotonia. In contrast, pathologic involvement at any point in the descending inhibitory paths leads to an exaggeration of spinal stretch reflexes and an increased resistance to manipulation of muscles and clonus, symptoms collectively called spasticity.
With tungsten microelectrodes percutaneously inserted into human peripheral nerve fascicles, in vivo recordings of single-unit action potentials can be obtained from different types of myelinated and unmyelinated nerve fibers. This technique of microneurography has provided a great deal of information about (1) the sensory innervation of the human skin, with its mechanoreceptive, thermoreceptive, and nociceptive functions, (2) the proprioceptive innervation of human skeletal muscles, special attention being devoted to the motor control functions of the muscle spindles and the fusimotor system, and (3) the sympathetic innervation of autonomic effector organs in skin and muscle, with its significance for, for example, regulation of temperature and blood pressure. The technique has its main application not as a routine procedure in clinical diagnostic work but as a research tool in basic physiologic and pathophysiologic studies.
A study has been made of the neurophysiological changes that follow spinal cord lesions in man. The Achilles tendon reflex (ATR) is used to estimate transmission in the Ia monosynaptic pathway, and the tonic vibration reflex (TVR) to estimate transmission in the Ia polysynaptic pathway to motoneurons. The inhibition of the H reflex by vibration is used as an estimate of presynaptic inhibition of the Ia monosynaptic pathway. Immediately following a complete lesion of the spinal cord presynaptic inhibition of the Ia monosynaptic pathway appears to be greatly increased. This enhanced inihibition may last several months but it eventually declines and in some instances becomes less than normal. Transmission in the Ia polysynaptic pathway is permanently abolished by a complete spinal lesion. A hypothesis is developed from these findings to explain the evolution of some of the clinical features that follow complete spinal lesions in man. Distinct differences are observed when the spinal lesion is incomplete. Transmission in the Ia polysynaptic pathway may be preserved and there may be no increase in presynaptic inhibition. These differences may depend upon the integrity of certain spinal long tracts which cannot be tested clinically.
The excitability of segmental reflex pathways in normal subjects and in patients with hemiplegia has been examined by conditioning the monosynaptic H reflex with a 200 msec burst of vibration applied to the tendo Achilles. In 6 normal subjects, the burst of vibration produced a short-latency facilitation of soleus motoneurons (attributed to monosynaptic excitation) which was followed by a longer-latency inhibition. A similar response was observed in 8 patients with hemiplegia, but the late inhibition was significantly less. The loss of an inhibitory mechanism may contribute to the exaggerated reflexes observed in patients with hemiplegia.
No single clinical electrophysiological test can evaluate disorders of muscle tone. These disorders, symptomatic of a variety of diseases have a multifactorial physiological basis. The several tests used are complimentary each aiming to study different aspects of spinal and supraspinal reflexes which become deranged. The H reflex and F wave (H max/M max and F max/M max ratios) measure motoneuron pool excitability in general. The tendon reflex includes spindle mechanisms bypassed by the H reflex and, with limitations, comparison of H max/M max and T max/M max yields information about the gamma system. Tonic vibration of a tendon inhibits the H reflex from the same muscle. The TVR measures autogenous presynaptic inhibition exerted by the Ia afferents of the muscle. Recurrent inhibition via Renshaw cells is evaluated by studying the effect of collision on the H reflex. Reciprocal inhibition of the Ia afferents can be assessed by measuring H reflex change induced by stimulating Ia afferents from antagonists. Changes in the H reflex recovery cycle measure polysynaptic influences on spinal motoneuron excitability. Cutaneo-muscular (flexor) reflexes measure poly- and oligosynaptic excitatory drive to spinal motoneurons and the blink reflex evaluates the excitatory drive to brainstem motoneurons. Long loop (segmental) responses can be evaluated by limb pertubation using a torque motor or electrical stimulation applied during voluntary muscle contraction. Finally needle electromyography is a more relevant test in several disorders of muscle tone such as the stiff-man syndrome and Isaacs' syndrome.
Lumbosacral spinal evoked potentials were recorded percutaneously in 22 MS patients with spinal symptoms and in 24 age-matched normal volunteers. Latencies, durations, and areas of waves R and A (level S1) as well as S and P2 (level Th12) were analyzed. The most significant result observed in the MS group was a reduction of the ratio between the areas of P2 and S. The reduction was strongly correlated with intensity of spasticity, but not with other clinical features. The P2/S ratio can thus be proposed as an electrophysiologic measure of spasticity.
Studies of decerebrate and spinal cats and monkeys as carried out by the authors over a number of years are reviewed. Factors responsible for early and late changes in reflex activity are considered. Hyperreflexia, as a late event, in chronic spinal animals is chiefly attributed to sprouting from afferent axons.Copyright © 1973 S. Karger AG, Basel
In 18 monkeys, unilateral ablation of areas 4 and 6 in precentral cortex resulted in an initial hypotonic hemiparesis which was succeeded in 4 to 6 wk by a hypertonic hemiparesis. In all animals there was some damage to the white matter underlying the ablation which affected fibres emerging from the supplementary motor area. Electromyographic examination of the responses to stretch of ankle extensor muscle showed a delay in onset of discharge in the hemiparetic hindlimb during the phase of hypotonic paresis and abrupt reversal with the onset of hypertonia, so that units in the hemiparetic limb responded to a lesser degree of extension than units in the control limb. Recordings of the responses of medial gastrocnemius spindle primary afferents to extension of this muscle were made at various stages after ablation of cortical areas 4 and 6 and the results compared with data similarly obtained from control animals and animals which had undergone section of the medullary pyramids. In the first week after cortical ablation, there was a significant depression of afferent responses, in relation both to control animals and to animals with medullary pyramidotomies. Two weeks after ablation, however, appreciable recovery of responses had occurred, though the responses remained less than those of controls. By the fourth to eighth week, when the animals had developed hypertonia of the affected limbs, spindle responses recovered to control levels but did not exceed them, though they were greater than the responses of animals with medullary pyramidotomies of similar duration. Spindle responses were thus depressed during the phase of hypotonic hemiplegia and recovered to control levels during the phase of hypertonic hemiplegia. It is suggested that the effects of cortical ablation represent an algebraic summation of the depressant effects of pyramidal lesions and the heightening effects of extrapyramidal lesions on fusimotor neurons. The hypertonia of this experimental model is not based upon a tonic heightening of fusimotor activity, since there is no evidence that spindle responses exceed control levels, even in strongly hypertonic animals.
1. The property of insect fibrillar muscle which enables it to oscillate continuously when it is connected to a resonant load is the delayed activation by stretch of contractile activity. The dynamic response has been measured at different fibre lengths and at different calcium ion concentrations, to see what effects these conditions have on the magnitude and rate constant of the delayed tension.
2. Bundles of ten fibres of the dorsal longitudinal muscle of the water bug, Lethocerus cordofanus , which had been in glycerol for less than 5 days were used. Graded activation was obtained with buffered calcium ion concentrations between 10 ⁻⁷ and 10 ⁻⁵ M .
3. A computer‐controlled apparatus was used to measure the dynamic mechanical properties of the muscle fibres. This allowed many measurements to be made on the same preparation. Further computer programs analysed the Nyquist plots produced by the experiment.
4. When the mean length of a fibre bundle was increased, the magnitude of the delayed tension was increased (for a constant amplitude of sinusoidal length change), the rate constant was unaltered, and the stiffness of the fibres was increased. When the calcium ion concentration was raised, the magnitude of the delayed tension was increased, the rate constant increased, and the stiffness of the fibres fell. Calcium activation and stretch activation are thus clearly separable in their effects, and so the mechanisms must be separate.
5. The various different effects of calcium cannot be explained by any simple model of activation, for example, an on‐off switch mechanism controlling the number of bridges in action.
6. The stretch‐induced activity is proportional to a power of the length of two or greater and this non‐linearity aids the efficient operation of the oscillatory mechanism.
Evaluation of the effects of treatment of patients with spasticity is complicated by reliance upon subjective estimates of the response of their muscles to passive stretch. An electronic system has been devised to record objective measurements of spasticity; the device moves the subject’s limb in a programed manner and records the resistance to the movement. During the movement, limb position, limb velocity, forces required to move the limb, and EMG data are recorded on a strip chart recorder and an XY recorder. Hysteresis loops reveal characteristic patterns for flexor and extensor resistance and for mixed flexorextensor syndromes. Studies are described of the range of variation encountered on repeated measurements in ten normal subjects and nine patients with hemiplegia.
The reflex response to stretch has been studied in the upper limb of 20 spastic patients. The amplitude of reflex EMG was found to be closely related to the velocity of stretch. Reflex EMG in biceps and triceps muscles was augmented by increasing the length of the muscle, although minimal inhibition of reflex EMG in biceps was obtained in two patients by extreme stretch. The clasp-knife sensation in the upper limb cannot be related to autogenic inhibition but may be explained by the characteristics of a velocity-dependent reflex in which limb movement is braked by the mechanical effect of increasing muscle tension. It is suggested that this be called the pseudo-clasp-knife reaction to distinguish it from the clasp-knife phenomenon of the quadriceps muscle, since the underlying neurophysiological mechanism is quite different.