**Abstract**

This chapter presents the technology of spasticity treatment—from diagnosis and treatment to quality control of treatment and rehabilitation. The diagnosis is based on methods of manual testing and differential diagnosis of spastic muscles, methods of quantitative assessment of spasticity on the basis of the Tardieu scale. The methodical development of the Tardieu scale with variants of its full and reduced use is presented. The basic patterns of spasticity of the upper and lower limbs are given. Schemes of management of patients with spasticity with indication of control points for application of methods of an assessment that shows efficiency of treatment and rehabilitation are presented. The methodology of spasticity treatment using botulinum neurotoxin (BoNT), including ultrasonic navigation, orientation of intramuscular motor endpoint of muscles (IME), is described. IME location diagrams and ultrasound picture of muscles are presented. Scales are proposed to assess the effect of spasticity on the functions of the upper and lower limbs. In conclusion, a variant of complex treatment of spasticity and original patient models are proposed, the use of which makes it possible to calculate the cost of BoNT.

**Keywords:** spasticity, patterns of spasticity, testing of spastic muscles, modified Tardieu scale (MTS), botulinum neurotoxin (BoNT), ultrasonic navigation, intramuscular motor endpoint (IME), rehabilitation

### **1. Introduction**

Spasticity as the most important component of the defeat syndrome of the upper motor neuron is a motor disorder characterized by a speed-dependent increase in tonic stretching reflexes (muscle tone) with increased tendon reflexes, due to hyperexcitability of the stretching reflex, as one of the components of the syndrome [1]. It is detected in more than 12 million people in the world and is the cause of disability in 12–27% of them [2, 3]. The list of nosological forms in which the structure of the injury syndrome in the *upper motor neuron lesion* (UMNL) observed spastic hypertonicity is significant. It is determined in approximately 20–40% of stroke survivors, 14% of traumatic brain injury survivors, 65–78% of patients with spinal cord lesions, and 85% of patients with multiple sclerosis [4, 5].

Spasticity is a major obstacle to the recovery of the patients who have suffered brain damage. The work of restoring movement becomes impossible with the unresolved issue of spasticity, the treatment of which expands the frame of "the rehabilitation window" and defines the rehabilitation terms. In addition, in the absence of spasticity treatment, the risk of paresis complications increases: contractures, bedsores, limb deformities, pain, muscle spasms, etc. [6].

• the start of the physiological mechanisms of spasticity by activating muscle antagonists (taping, magnetic, electric stimulation, etc.) and initiating the mechanism of reciprocal interaction (kinesitherapy and other techniques);

• the use of methods that enable balancing the activity phases of the movement by reducing the activity in the 1st phase, up to severity 2nd (BoNT injections,

The most common complications of spasticity are contractures. They, together with spasticity, serve as the main obstacle to rehabilitation measures. The most common are the contractures of the shoulder (86%) and ankle (19%) joints. Adaptogenes of these contractures is different. Ankle contracture occurs among patients with late motor activity, severe paresis (70%), low motivation (81%), and incorrect treatment (23%). In contrast, shoulder contracture in 71% of cases is caused by the activity and verticalization of the patient in the first 14 days after the stroke. The shoulder joint, having the largest volume of movements, completely assumes all weight of the upper limb. With paresis and initial hypotension, often occurring after a stroke, the entire weight of the arm (4–7 kg) falls on the ligamentous apparatus of the joint, its articular bag, causing their trauma and pain. This, in turn, leads to the progressing severity of spasticity, as well as periarticular and

By 6 months after the stroke, 90% of cases of spasticity, 36% of joint contractures, and 57% of tendon-muscle contractures (internal spasticity) are formed. At the same time, of all cases of spasticity, the manifestation of its signs in 77.3% of patients falls on the first 2–3 weeks. As a rule, the severity of spasticity in the first 2 weeks does not exceed 1–2 points on the Modified Ashworth scale (MAS). Increased spasticity by 1-point MAS increases the consumption of botulinum neurotoxin (BoNT) by 100–200 Units, which significantly increases the cost of treatment. Thus, early detection and treatment of spasticity reduces the cost of therapeutic

In the muscles involved in the spasticity pattern, diffuse muscle changes (DMC) develop over time in a form of connecting tissue substitution. There are no clear time criteria for the development of DMC. Among many patients with a disease duration of more than 4 years, the muscle structure is preserved. Some DMC develop within 6 months. Clinical signs of DMC are the following: low tissue turgor, decreased muscle volume, and significant restriction of movement, up to its total absence. While ultrasounding such muscles, in addition to reducing the volume, a

Currently, a classification has been adopted in which generalized, regional, and

focal forms of spasticity are distinguished. There are also patterns of spasticity characteristic of different joints and muscles of the upper and lower limbs. Depending on the form and pattern of spasticity, the strategy and tactics of its

• spasticity with marked para- or tetraparesis—intrathecal baclofen [15].

For effective treatment of spasticity with BoNT drugs, it is necessary to determine the spasticity pattern with verification of the muscles that form it; and then

• generalized spasticity with pain—сentral muscle relaxants;

stretching).

*Spasticity: Diagnosis and Treatment*

*DOI: http://dx.doi.org/10.5772/intechopen.91046*

articular changes [13].

rehabilitation measures [13, 14].

treatment are determined [10]:

**51**

hyperechogenic signal is registered (**Figure 1**) [17].

• focal and segmental spasticity—drugs BoNT;

their correct introduction into the target muscle.

The development of spasticity is directly related to the initial stages of recovery of movement in paretic limbs. In 1–3 weeks after UMNL, the connections of the cerebral cortex with the structures of the extrapyramidal system (EPS) begin to recover. Recovery time varies depending on the degree of damage: from 2 weeks to 3 months [7].

During this period, the initiation of movements, in accordance with their image in the associative cortex, is able to be realized through intact EPS pathways. This efferent flow, reaching α-small motor neurons (MN), increases the tone in the muscles innervated by them (1st movement phase) for subsequent implementation of the dynamic phase (2-phase motion). However, the latter does not receive a sufficiently powerful efferentation due to the continuing defective functioning of the pyramid path. The result of this is the lack of inclusion of a sufficient number of inhibitory cells (Renshaw), which could inhibit α-small MN and lower muscle tone [7, 8].

Spasticity in strokes is usually formed in the first 3 months after the vascular accident. Its first signs usually begin to appear by the beginning of the 3rd week. The process of spasticity development is quite dynamic and variable. The terms of spasticity development from the first signs of tonus increase to the formed pattern in 2–5 weeks [9–11].

The development of spastic syndrome depends on many reasons: pain, stress, violation of proprioception, violation of the image of the body scheme and balance, tension and phobias with instability in a sitting or walking position.

Pain syndrome has a special place in the development of spasticity. For example, pain in the shoulder joint is directly associated with the development of spasticity. The absence of pain or its temporary relief in 83% of cases reduces the severity of spasticity.

Instability and uncertainty when walking, as well as stress, significantly affect the development of spasticity in the upper limb. So, spasticity in the hand, often develops in patients with severe weakness of the lower limb who retained the ability to move. During the period of yet unformed pattern of spasticity, these patients begin to strain, bend, and bring paretic arm to maintain balance while walking, which in 3–4 weeks causes the formed pattern of spasticity of the upper limb [12–14].

An important role in the development of spasticity plays the violation of proprioception, which leads to the violation of the image of the body scheme. Lack of afferentation triggers mechanisms that should increase the power of information from the tendons and joints receptors. In the case of spasticity, when dynamic muscle contraction is impossible due to paresis, it leads to activation of spinal and supraspinal mechanisms of tonus enhancement [15, 16].

Thus, the main directions in the rehabilitation of the consequences injury to the upper motor neuron and in the treatment of spasticity are:

• creating conditions precluding the need for the injury. For this purpose, analgesics, anxiolytics, as well as special styling, exercise therapy and hardware techniques are used, which activate proprioception, forming an associative image of the body scheme;

### *Spasticity: Diagnosis and Treatment DOI: http://dx.doi.org/10.5772/intechopen.91046*

Spasticity is a major obstacle to the recovery of the patients who have suffered

The development of spasticity is directly related to the initial stages of recovery of movement in paretic limbs. In 1–3 weeks after UMNL, the connections of the cerebral cortex with the structures of the extrapyramidal system (EPS) begin to recover. Recovery time varies depending on the degree of damage: from 2 weeks

During this period, the initiation of movements, in accordance with their image in the associative cortex, is able to be realized through intact EPS pathways. This efferent flow, reaching α-small motor neurons (MN), increases the tone in the muscles innervated by them (1st movement phase) for subsequent implementation of the dynamic phase (2-phase motion). However, the latter does not receive a sufficiently powerful efferentation due to the continuing defective functioning of the pyramid path. The result of this is the lack of inclusion of a sufficient number

of inhibitory cells (Renshaw), which could inhibit α-small MN and lower

tension and phobias with instability in a sitting or walking position.

Spasticity in strokes is usually formed in the first 3 months after the vascular accident. Its first signs usually begin to appear by the beginning of the 3rd week. The process of spasticity development is quite dynamic and variable. The terms of spasticity development from the first signs of tonus increase to the formed pattern

The development of spastic syndrome depends on many reasons: pain, stress, violation of proprioception, violation of the image of the body scheme and balance,

Pain syndrome has a special place in the development of spasticity. For example, pain in the shoulder joint is directly associated with the development of spasticity. The absence of pain or its temporary relief in 83% of cases reduces the severity

Instability and uncertainty when walking, as well as stress, significantly affect the development of spasticity in the upper limb. So, spasticity in the hand, often develops in patients with severe weakness of the lower limb who retained the ability to move. During the period of yet unformed pattern of spasticity, these patients begin to strain, bend, and bring paretic arm to maintain balance while walking, which in 3–4 weeks causes the formed pattern of spasticity of the upper limb

An important role in the development of spasticity plays the violation of proprioception, which leads to the violation of the image of the body scheme. Lack of afferentation triggers mechanisms that should increase the power of information from the tendons and joints receptors. In the case of spasticity, when dynamic muscle contraction is impossible due to paresis, it leads to activation of spinal and

Thus, the main directions in the rehabilitation of the consequences injury to the

analgesics, anxiolytics, as well as special styling, exercise therapy and hardware techniques are used, which activate proprioception, forming an associative

• creating conditions precluding the need for the injury. For this purpose,

supraspinal mechanisms of tonus enhancement [15, 16].

image of the body scheme;

upper motor neuron and in the treatment of spasticity are:

brain damage. The work of restoring movement becomes impossible with the unresolved issue of spasticity, the treatment of which expands the frame of "the rehabilitation window" and defines the rehabilitation terms. In addition, in the absence of spasticity treatment, the risk of paresis complications increases: contractures, bedsores, limb deformities, pain, muscle spasms, etc. [6].

*Neurostimulation and Neuromodulation in Contemporary Therapeutic Practice*

to 3 months [7].

muscle tone [7, 8].

in 2–5 weeks [9–11].

of spasticity.

[12–14].

**50**


The most common complications of spasticity are contractures. They, together with spasticity, serve as the main obstacle to rehabilitation measures. The most common are the contractures of the shoulder (86%) and ankle (19%) joints. Adaptogenes of these contractures is different. Ankle contracture occurs among patients with late motor activity, severe paresis (70%), low motivation (81%), and incorrect treatment (23%). In contrast, shoulder contracture in 71% of cases is caused by the activity and verticalization of the patient in the first 14 days after the stroke. The shoulder joint, having the largest volume of movements, completely assumes all weight of the upper limb. With paresis and initial hypotension, often occurring after a stroke, the entire weight of the arm (4–7 kg) falls on the ligamentous apparatus of the joint, its articular bag, causing their trauma and pain. This, in turn, leads to the progressing severity of spasticity, as well as periarticular and articular changes [13].

By 6 months after the stroke, 90% of cases of spasticity, 36% of joint contractures, and 57% of tendon-muscle contractures (internal spasticity) are formed. At the same time, of all cases of spasticity, the manifestation of its signs in 77.3% of patients falls on the first 2–3 weeks. As a rule, the severity of spasticity in the first 2 weeks does not exceed 1–2 points on the Modified Ashworth scale (MAS). Increased spasticity by 1-point MAS increases the consumption of botulinum neurotoxin (BoNT) by 100–200 Units, which significantly increases the cost of treatment. Thus, early detection and treatment of spasticity reduces the cost of therapeutic rehabilitation measures [13, 14].

In the muscles involved in the spasticity pattern, diffuse muscle changes (DMC) develop over time in a form of connecting tissue substitution. There are no clear time criteria for the development of DMC. Among many patients with a disease duration of more than 4 years, the muscle structure is preserved. Some DMC develop within 6 months. Clinical signs of DMC are the following: low tissue turgor, decreased muscle volume, and significant restriction of movement, up to its total absence. While ultrasounding such muscles, in addition to reducing the volume, a hyperechogenic signal is registered (**Figure 1**) [17].

Currently, a classification has been adopted in which generalized, regional, and focal forms of spasticity are distinguished. There are also patterns of spasticity characteristic of different joints and muscles of the upper and lower limbs. Depending on the form and pattern of spasticity, the strategy and tactics of its treatment are determined [10]:


For effective treatment of spasticity with BoNT drugs, it is necessary to determine the spasticity pattern with verification of the muscles that form it; and then their correct introduction into the target muscle.

### **Figure 1.**

*Ultrasound picture of normal muscle tissue (a) and muscles with hyperechogenic ultrasonic signal due to DMC (b).*

Twelve main clinical patterns of spasticity for the upper (5) and lower (7) limbs have been identified. Spasticity patterns for the hands include various, mainly flexor, variants of flexion in the joints: retracting the shoulder, elbow flexion, forearm pronation, wrist flexion, and finger flexion [18]. Spasticity patterns for the leg consist of hip reduction, knee flexion, knee extension, plantar flexion of the foot, equinovarus positioning of the foot, flexion of the fingers, and extension of the thumb [19].

## **2. Clinical diagnostic of spasticity**

### **2.1 Manual testing of muscles for spasticity**

Muscle testing is required to identify specific muscles involved in the spasticity pattern. All spastic muscle testing methods are based on two principles:

lifting of the shoulder, and its supination. Almost all the muscles of the shoulder girdle can influence these movement vectors, but most often it is done by the following: *m. Pectoralis* major (PM) (90%), *m. Subscapularis* (S/s) (20%), and

axillary cavity, respectively). Diagnosis is done visually and by palpation.

Spasticity PM and LD is diagnosed when the shoulder is raised and withdrawn with the express tension of their lateral edge (the anterior and posterior walls of the

S/s retracts the shoulder and rotates it inward. Spasticity is diagnosed by lifting, retraction and supination of the shoulder by visual and palpatory control of the lower angle and medial edge of the scapula. Normally, the shoulder is withdrawn without moving the blade to the horizontal level (80–90°). Thus, if the movement of the blade begins before reaching this level, there is an increase in tone in S/s. There is individual variability, so it is necessary to compare this movement with the

**Elbow flexors.** The main muscles flexing the elbow are mm. Brachioradialis (BR), Brachialis (Br), and Biceps brachii (BB) (muscles are listed by importance in the spasticity pattern). BB is also a powerful arch support of the forearm. The muscles are tested when provoking a stretch reflex (muscle stretching reflex, mitotic reflex) at different rates of extension in the elbow joint. The reaction of BR and BB is evaluated visually and by palpation (**Figures 4** and **5**). The reaction of Br can only be assessed by palpation, gripping, with your own fingers upon humerus

*m. Laissimus dorsi* (LD) (5%).

*M. Subscapularis spasticity testing.*

**Figure 2.**

**Figure 3.**

*Types of upper limb spasticity patterns [16].*

*Spasticity: Diagnosis and Treatment*

*DOI: http://dx.doi.org/10.5772/intechopen.91046*

intact hand (**Figure 3**).

**53**


For spasticity patterns in the arm, an anatomical description is used with a representation of all the muscles that could perform a given movement in the joints (**Figure 2**). For differentiation of compensatory inclusions of muscles, it is necessary after definition of type of a pattern of spasticity in a hand to carry out manual testing.

### *2.1.1 Upper limb muscle testing*

**Bringing and pronation of the shoulder.** At the heart of the restriction of movements in the shoulder with spasticity are problems with the withdrawal,

**Figure 2.** *Types of upper limb spasticity patterns [16].*

**Figure 3.** *M. Subscapularis spasticity testing.*

Twelve main clinical patterns of spasticity for the upper (5) and lower (7) limbs

Muscle testing is required to identify specific muscles involved in the spasticity

2.Differentiation of movements for muscles with the same function, but passing

1. Identification and activation of exclusive and additional functions of the

For spasticity patterns in the arm, an anatomical description is used with a representation of all the muscles that could perform a given movement in the joints (**Figure 2**). For differentiation of compensatory inclusions of muscles, it is necessary after definition of type of a pattern of spasticity in a hand to carry out

**Bringing and pronation of the shoulder.** At the heart of the restriction of movements in the shoulder with spasticity are problems with the withdrawal,

pattern. All spastic muscle testing methods are based on two principles:

have been identified. Spasticity patterns for the hands include various, mainly flexor, variants of flexion in the joints: retracting the shoulder, elbow flexion, forearm pronation, wrist flexion, and finger flexion [18]. Spasticity patterns for the leg consist of hip reduction, knee flexion, knee extension, plantar flexion of the foot, equinovarus positioning of the foot, flexion of the fingers, and extension

*Ultrasound picture of normal muscle tissue (a) and muscles with hyperechogenic ultrasonic signal due to*

*Neurostimulation and Neuromodulation in Contemporary Therapeutic Practice*

of the thumb [19].

**Figure 1.**

*DMC (b).*

studied muscle.

*2.1.1 Upper limb muscle testing*

manual testing.

**52**

**2. Clinical diagnostic of spasticity**

**2.1 Manual testing of muscles for spasticity**

through a different number of joints.

lifting of the shoulder, and its supination. Almost all the muscles of the shoulder girdle can influence these movement vectors, but most often it is done by the following: *m. Pectoralis* major (PM) (90%), *m. Subscapularis* (S/s) (20%), and *m. Laissimus dorsi* (LD) (5%).

Spasticity PM and LD is diagnosed when the shoulder is raised and withdrawn with the express tension of their lateral edge (the anterior and posterior walls of the axillary cavity, respectively). Diagnosis is done visually and by palpation.

S/s retracts the shoulder and rotates it inward. Spasticity is diagnosed by lifting, retraction and supination of the shoulder by visual and palpatory control of the lower angle and medial edge of the scapula. Normally, the shoulder is withdrawn without moving the blade to the horizontal level (80–90°). Thus, if the movement of the blade begins before reaching this level, there is an increase in tone in S/s. There is individual variability, so it is necessary to compare this movement with the intact hand (**Figure 3**).

**Elbow flexors.** The main muscles flexing the elbow are mm. Brachioradialis (BR), Brachialis (Br), and Biceps brachii (BB) (muscles are listed by importance in the spasticity pattern). BB is also a powerful arch support of the forearm. The muscles are tested when provoking a stretch reflex (muscle stretching reflex, mitotic reflex) at different rates of extension in the elbow joint. The reaction of BR and BB is evaluated visually and by palpation (**Figures 4** and **5**). The reaction of Br can only be assessed by palpation, gripping, with your own fingers upon humerus

are progressively flexed as the hand is extended, this means that neither of the two flexors of the hand (m. Flexor carpi radialis and m. Flexor carpi ulnaris) participates in its flexion. Pathological flexion of the hand in this case is due to spasticity m. Flexor digitorum profundus (FDP) and m. Flexor digitorum superficialis (FDS)

In order to distinguish spasticity in FDS and FDP, you can extend the wrist joint.

If manipulations in the wrist joint did not have any effect on the position of the thumb, it means that the muscles of the hand are responsible for its position: mm.

In this movement, it is necessary to pay attention to the proximal and distal interphalangeal joints of the fingers. If it is found that the distal interphalangeal joints are bent to a greater extent, this indicates the spasticity of the deep flexor of

the fingers. If the proximal interphalangeal joints-superficial flexor fingers (**Figure 8**). If this bends the distal phalanx of the thumb—this indicates spasticity

Flexor pollicis brevis, Opponens pollicis Adductor pollicis (**Figure 10**).

*M. Flexor digitorum profundus и m. Flexor digitorum superficialis spasticity testing.*

*Differential diagnosis of spasticity m. Flexor digitorum profundus and m. Flexor digitorum superficialis.*

(**Figure 7**).

**Figure 7.**

**Figure 8.**

**55**

m. Flexor pollicis longus (**Figure 9**).

*Spasticity: Diagnosis and Treatment*

*DOI: http://dx.doi.org/10.5772/intechopen.91046*

**Figure 4.** *M. Biceps brachii spasticity testing.*

**Figure 5.** *M. Brachialis spasticity testing.*

**Figure 6.** *M. Brachioradialis spasticity testing.*

from below (rear). Win case of spasticity in response to a sharp extension in the elbow joint under the fingertips you feel tension (**Figure 6**).

**Forearm pronators.** Forearm pronates three muscles: mm. Pronator teres (PT) and Pronator quadratus (PQ) and m. Flexor carpi radialis (FCR). PT and FCR in pronation act as a single functional unit. In some cases, with ultrasound of these muscles, you can find the lack of a clear boundary between them, which once again confirms the generality of their function. Testing these two muscles is based on provoking the stretch reflex in response to rapid supination. The presence of spasticity in FCR is manifested visually and confirmed by palpation. Spasticity in PT can be determined only by palpation, putting your fingers on the middle line of the forearm 2–4 cm below the elbow bend and producing supination. Sometimes when assessing pronator spasticity, FCR is more stressful than PT.

**Flexors of the hand and fingers.** Testing is performed by back flexion in the wrist joint. If no significant resistance is felt during this movement, and the fingers

### *Spasticity: Diagnosis and Treatment DOI: http://dx.doi.org/10.5772/intechopen.91046*

are progressively flexed as the hand is extended, this means that neither of the two flexors of the hand (m. Flexor carpi radialis and m. Flexor carpi ulnaris) participates in its flexion. Pathological flexion of the hand in this case is due to spasticity m. Flexor digitorum profundus (FDP) and m. Flexor digitorum superficialis (FDS) (**Figure 7**).

In order to distinguish spasticity in FDS and FDP, you can extend the wrist joint. In this movement, it is necessary to pay attention to the proximal and distal interphalangeal joints of the fingers. If it is found that the distal interphalangeal joints are bent to a greater extent, this indicates the spasticity of the deep flexor of the fingers. If the proximal interphalangeal joints-superficial flexor fingers (**Figure 8**). If this bends the distal phalanx of the thumb—this indicates spasticity m. Flexor pollicis longus (**Figure 9**).

If manipulations in the wrist joint did not have any effect on the position of the thumb, it means that the muscles of the hand are responsible for its position: mm. Flexor pollicis brevis, Opponens pollicis Adductor pollicis (**Figure 10**).

**Figure 7.** *M. Flexor digitorum profundus и m. Flexor digitorum superficialis spasticity testing.*

**Figure 8.** *Differential diagnosis of spasticity m. Flexor digitorum profundus and m. Flexor digitorum superficialis.*

from below (rear). Win case of spasticity in response to a sharp extension in the

**Forearm pronators.** Forearm pronates three muscles: mm. Pronator teres (PT) and Pronator quadratus (PQ) and m. Flexor carpi radialis (FCR). PT and FCR in pronation act as a single functional unit. In some cases, with ultrasound of these muscles, you can find the lack of a clear boundary between them, which once again confirms the generality of their function. Testing these two muscles is based on provoking the stretch reflex in response to rapid supination. The presence of spasticity in FCR is manifested visually and confirmed by palpation. Spasticity in PT can be determined only by palpation, putting your fingers on the middle line of the forearm 2–4 cm below the elbow bend and producing supination. Sometimes when

**Flexors of the hand and fingers.** Testing is performed by back flexion in the wrist joint. If no significant resistance is felt during this movement, and the fingers

elbow joint under the fingertips you feel tension (**Figure 6**).

*Neurostimulation and Neuromodulation in Contemporary Therapeutic Practice*

**Figure 4.**

**Figure 5.**

**Figure 6.**

**54**

*M. Brachialis spasticity testing.*

*M. Brachioradialis spasticity testing.*

*M. Biceps brachii spasticity testing.*

assessing pronator spasticity, FCR is more stressful than PT.

• Valgus or varus.

*Spasticity: Diagnosis and Treatment*

• Adduction.

• Adduction.

• Of equinus.

• "Triple flexion".

• Flexion of the toes.

• Dynamic pattern.

**57**

• Adduction.

• Flexion of the ankle joints.

• Static pattern (equinovarus)

extensibility not associated with spasticity) [18].

4.Patterns of spasticity in stroke and brain injury.

• their combination with flexion of the toes.

• Exterior turn stop.

*DOI: http://dx.doi.org/10.5772/intechopen.91046*

2.Patterns of spasticity in multiple sclerosis.

• Flexion or extension of the hip.

• Flexion or extension of the knee.

3. Spasticity patterns in severe brain injury, encephalitis, and spinal injury.

Testing of the muscles of the lower limb is carried out in the supine position, on both limbs, consistently comparing flexion in the joints (to identify poor muscle

There are two main types of lower limb spasticity patterns in patients undergoing stroke: dynamic pattern (DP) and static pattern (SP), as well as their possible combinations with flexion of the toes and hip reduction. Patterns are proposed based on the principle of visual assessment of the limb position at rest and when walking [19]. In case DP manifestations of spasticity are determined only in the process of movement. In the resting position, the legs do not differ from healthy and its normal statics is kept (limb are visually full length, the joints are in the middle position, and toes are separated), the position of the fingers most often corresponds with the finger of these intact side. Walking is characterized by a peculiar pattern, in which in the phase of hip transfer and knee extension, before lowering the foot to the surface, there are oscillatory movements of the shin from side to side with possible flexion of the fingers. The cause of DP is increased tone and muscle-tendon contraction in the

muscles of the back of the thigh (hamstrings), mm. Semitendinosus (S/t), Semimembranosus (S/m), Biceps femoris (BF) and in *M. gracilis* (G).

Gait peculiarity in this type of spasticity is associated with the phylogenetic foundations of neurophysiology of movement in providing the act of walking and is

### **Figure 9.** *M. Flexor pollicis longus spasticity testing.*

### **Figure 10.**

*Patterns in spasticity of the muscles of the hand. (A) m. Flexor pollicis longus, (B) m. Flexor pollicis brevis, (C) m. Adductor pollicis, and (D) m. Opponens pollicis.*
