Muscle tone is a state of tension that is maintained continuously – minimally even when relaxed – and which increases in resistance to passive stretch. It helps to maintain posture and decreases during sleep. The stretch reflex is a muscle contraction in response to stretching within the muscle. This reflex, by definition extremely fast exists to allow the muscle to adapt to any kind of muscular tone, to avoid over-stretching , e.g. when need to adapt to a brutal change of the ground.

In spasticity, the muscle tone is abnormally increased (muscle hypertonia), and reflexes such as the stretch reflex may persist for too long and may be too strong (hyperactive reflexes). These phenomena cause an increased resistance to passive movement (e.g., if someone else tries to move the extremities of the person affected) characterized in the following ways:

1. it increases with increasing speed of stretch and varies with the direction of joint movement and/or
2. it increases above a patient-specific threshold speed or joint angle

The slower the speed and the smaller the angle when spasticity appears, the more severe it is.

Diagnosis of spasticity is mainly based on clinical evaluation that should include:

• Clinical history
• Physical examination
• evaluation of stretch reflexes (e.g., deep tendon reflexes, involuntary muscle contractions provoked by stretching the muscle with a tap on the tendon that connects the muscle to a bone)
• passive and active motion
• Function, e.g., toileting, eating, sleeping, dressing, sitting, standing, and walking

A proper assessment of the individual’s clinical and neurological status is critical in developing an effective treatment plan with achievable goals.

Spasticity is diagnosed if the patient shows an increased resistance to passive movements that increases with speed and typical positioning of the limbs, due to increased muscle tone. The diagnosis is not complicated for rehabilitation specialists but unfortunately a lot of other specialists/HCP are not trained and thus don’t recognized the symptoms or when they do so, don’t see the potential benefit of an adapted treatment.

Spasticity is diagnosed if the patient shows an increased resistance to passive movements that increases with speed and typical positioning of the limbs, due to increased muscle tone. The diagnosis is not complicated for rehabilitation specialists but unfortunately a lot of other specialists/HCP are not trained and thus don’t recognized the symptoms or when they do so, don’t see the potential benefit of an adapted treatment.

Diagnosis of spasticity is mainly based on clinical evaluation that should include:

• Clinical history
• Physical examination
• evaluation of stretch reflexes (e.g., deep tendon reflexes, involuntary muscle contractions provoked by stretching the muscle with a tap on the tendon that connects the muscle to a bone)
• passive and active motion
• Function, e.g., toileting, eating, sleeping, dressing, sitting, standing, and walking

A proper assessment of the individual’s clinical and neurological status is critical in developing an effective treatment plan with achievable goals.

Spasticity is diagnosed if the patient shows an increased resistance to passive movements that increases with speed and typical positioning of the limbs, due to increased muscle tone. The diagnosis is not complicated for rehabilitation specialists but unfortunately a lot of other specialists/HCP are not trained and thus don’t recognized the symptoms or when they do so, don’t see the potential benefit of an adapted treatment.

The features of spasticity should be assessed individually for each patient, with the focus on three main areas: The clinical pattern of motor function, the patient’s ability to control his or her muscles, and how muscle stiffness and any contractures worsen the functional problems. The clinical pattern is of particular interest as it helps to identify the muscles affected by spasticity and thus to determine an appropriate treatment. Some physicians use diagnostic nerve blocks (local transient anesthesia of nerve(s)) to evaluate the involvement of muscles in a specific spastic pattern), or electromyography (EMG, evaluating activity of muscles while the patient performs a movement or a task via external electrodes).

Post-stroke spasticity is usually diagnosed and treated at rehabilitation centers, where many experts, such as, rehabilitation specialists, occupational therapists, physical therapists, speech therapists, psychologists, social workers, nurses…, work together to provide patients with different treatment options.

Spasticity can occur in the upper and lower limbs. The body region and the extent to which it is affected depend on the area of the brain or spinal cord that has been damaged.

• In spastic hemiplegia, the muscles of one side of the body are affected. Generally, injury to the left side of the brain will cause symptoms in the right side of the body, and vice versa. Hemiparesis is weakness on one side of the body. It is less severe than hemiplegia. Thus, the patient can move the impaired side of their body, but with reduced muscular strength.
• In patients with spastic diplegia, most often the lower limbs are affected, called then paraplegia. In that case, it is mainly related to a lesion of the spinal cord. Rarely diplegia concerns the 2 upper limbs.
• All four limbs are affected in patients with spastic quadriplegia. These patients are the least likely to be able to walk. This is mainly related to lesion of the spinal cord.

Diagnosis of spasticity is mainly based on clinical evaluation that should include:

• Clinical history
• Physical examination
• evaluation of stretch reflexes (e.g., deep tendon reflexes, involuntary muscle contractions provoked by stretching the muscle with a tap on the tendon that connects the muscle to a bone)
• passive and active motion
• Function, e.g., toileting, eating, sleeping, dressing, sitting, standing, and walking

A proper assessment of the individual’s clinical and neurological status is critical in developing an effective treatment plan with achievable goals.

Spasticity is diagnosed if the patient shows an increased resistance to passive movements that increases with speed and typical positioning of the limbs, due to increased muscle tone. The diagnosis is not complicated for rehabilitation specialists but unfortunately a lot of other specialists/HCP are not trained and thus don’t recognized the symptoms or when they do so, don’t see the potential benefit of an adapted treatment.

The features of spasticity should be assessed individually for each patient, with the focus on three main areas: The clinical pattern of motor function, the patient’s ability to control his or her muscles, and how muscle stiffness and any contractures worsen the functional problems. The clinical pattern is of particular interest as it helps to identify the muscles affected by spasticity and thus to determine an appropriate treatment. Some physicians use diagnostic nerve blocks (local transient anesthesia of nerve(s)) to evaluate the involvement of muscles in a specific spastic pattern), or electromyography (EMG, evaluating activity of muscles while the patient performs a movement or a task via external electrodes).

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38% of stroke survivors experience post-stroke spasticity within one year after a first stroke.

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The treatment of adult with spasticity should be provided by a multidisciplinary team employing a shared-care approach. A variety of treatment options is available and clinical experience has shown that a multi-modal approach has many benefits.  In most cases, a combination of various types of treatment is required to achieve the specific goals of treatment for a particular patient.

A rehabilitation plan must be tailored to individual patient needs, and is likely to involve medical intervention (e.g., botulinum toxin, pain medication), as well as multiple additional therapies – for example physical, occupational and psychological approaches. Together, these therapies enable optimal management of functional problems such as impaired mobility, strength, balance, and endurance, amongst other spasticity-related issues.

The primary aim of treatment is to facilitate life for people with spasticity and for their caregivers, thus improving their quality of life. Therefore, improvement in function is a key long-term factor in spasticity management. Consequently, the development of realistic and clinically relevant goals for each individual patient is the key for a successful treatment. These goals should  be defined  and  followed  up in collaboration with other members  of the  spasticity management team that  may include a specialist for physical medicine and rehabilitation, a neurologist, a physiatrist, a physiotherapist, an occupational therapist, a neurosurgeon, and an orthotist  (specialist concerned with the design,  manufacture and application  of orthoses).

The importance of adapting the treatment to patients’ symptoms and especially to patients’ needs throughout the course of treatment is crucial, with expectations revisited and redefined if necessary at regular intervals.

38% of stroke survivors experience post-stroke spasticity within one year after a first stroke, while the overall prevalence of post-stroke spasticity is approximately 0.2% (taken from the WHO MONICA project)

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Botulinum toxin type A (BoNT/A) is recommended as a first-line therapy in national and international guidelines as part of an integrated treatment approach for post-stroke spasticity.

Botulinum toxin creates a ‘window of opportunity’ for improving motor and activity performance3 and should always be followed by physical therapy.

Physical therapy is the mainstay of treatment for spasticity, and is designed to reduce muscle tone, maintain or improve range of motion and mobility, increase strength and coordination, and improve care and comfort.

When not controllable by physical therapy, oral or intrathecal medications and/or botulinum toxin injections, spasticity symptoms can be treated with selective ablative procedures. In most cases, complementary neurosurgical and functional orthopedic approaches are used.

With surgical interventions, muscles can be denervated or tendons and muscles can be released, lengthened, or transferred to relieve the symptoms of spasticity. In practice, only 5% of spasticity patients undergo a surgical intervention.

By orthopedic surgery, muscles can be denervated, and tendons and muscles can be released, lengthened, or transferred. In order to release contractures, the contracted tendon is partially or completely split surgically and then the joint is repositioned at a more normal angle.  A cast stabilizes the joint over a period of several weeks while the tendon regrows.  After removing the cast, physical therapy is necessary to strengthen the muscles and improve the patient’s range of motion.

Surgical intervention that is used for the treatment of spasticity is called functional or selective dorsal rhizotomy (SDR). In this procedure, the neurosurgeon  cuts nerve roots (rhizotomy) – the nerve fibers lying just outside  the back bone  (spinal column) that  send sensory messages from the muscles to the spinal cord. ‘Selective’  indicates that  only certain  nerve roots are cut, and ‘dorsal’ refers to the target  nerves that  are located  at the back of the spinal cord (the upper  surface  when  a person  is lying on his or her stomach).

Spasticity is one of several clinical features/motor behaviors that may result following damage to the part of the brain or spinal cord involved in controlling voluntary movement. Collectively, these features are known as the upper motor neuron (UMN) syndrome. Spasticity is associated with a pathologically increased muscle tone. This creates stiffness and resistance to passive movement (the word ‘spasm’ originates from the Greek word, ‘spasmos’, which means to drag or pull). This change in muscle tone may increase the disability related to the disease at the origin of spasticity.

Spasticity is one of the features of upper motor neuron (UMN) syndrome. UMN syndrome is caused by damage to one (or more) areas of the central nervous system (CNS) involved in controlling voluntary movement. UMN syndrome can be divided into two broad groups – negative phenomena and positive phenomena.

Negative phenomena refer to what is lost, such as fine motor skills, strength, and motor control.

Positive phenomena are characterized by an abundance of muscle hyperactivity, such as spasticity, hypereflexia (increased stretch reflexes), clonus (uncontrollable movement of a body limb, especially the ankle), co-contractions (involuntary contractions of a limb or a part of the limb while the patient is actively moving another part (e.g., lower limb) (e.g., adduction of the shoulder while walking), or muscles spasms.

38% of stroke survivors experience post-stroke spasticity within one year after a first stroke.

Spasticity is one of several clinical features/motor behaviors that may result following damage to the part of the brain or spinal cord involved in controlling voluntary movement. Collectively, these features are known as the upper motor neuron (UMN) syndrome. Spasticity is associated with a pathologically increased muscle tone. This creates stiffness and resistance to passive movement (the word ‘spasm’ originates from the Greek word, ‘spasmos’, which means to drag or pull). This change in muscle tone may increase the disability related to the disease at the origin of spasticity.