**1. Introduction**

#### **1.1 Human motricity and the impact of spinal cord injury**

There are three forms of human motricity: voluntary, involuntary, and reflex. Voluntary motricity is represented by the pyramidal system. Cortical motor cells and their extensions form the corticospinal pathway. The motor system is bineuronal and extends from the cerebral cortex to the myoneural junction. The first neuron (central motor neuron) has its cell body in the cerebral cortex from where its axon goes out. Synaptic endings occur in the anterior roots of the spinal cord, where they connect with the second neuron (peripheral motor neuron). This is the so-called pyramidal path. The axons of the pyramidal path pass through the oval center, the inner capsule, and arrive in the brainstem where most of their fibers cross the midline. These axons follow along with the lateral cord of the spinal cord and end up connecting the peripheral motor neuron in the anterior root of the spinal cord.

Involuntary motricity involves the extrapyramidal system. Cell bodies stem from the various nuclei of the base and are associated with areas of the motor cortex,

pre-motor, and subthalamic nuclei. There are several paths such as rubrospinal, reticulospinal, vestibulospinal, and cephalospinal paths. The extrapyramidal system and its pathways harmonize the voluntary motor system, guarantee the automatic motricity, and control the postural reflexes of spinal and vestibulocerebellar origins.

Reflex motricity depends on the pyramidal and extrapyramidal systems and represents only a few spinal reflexes.

Peripheral motor neurons are part of the peripheral nervous system (PNS) and are organized into motor units. Nerve fibers protract from the anterior roots of the spinal cord to muscle fibers and organs of muscular proprioception called muscle spindles. The spindles send sensorial signals to the spinal cord, informing the central nervous system (CNS) about the level of muscle contraction.

The CNS triggers nerve impulses that travel along the motor neuron toward the muscle fiber so that contraction can happen. They can excite the neuronal membrane to reach depolarization voltage levels above a triggering threshold that generates a particular wave known as action potential (AP). The AP consistently propagates along the axon toward the synaptic ending. At the synaptic cleft, vesicles deliver the neurotransmitter acetylcholine that connects to cholinergic receptors and depolarizes the myoneural junction. Eventually, the depolarization can generate a new AP that propagates along the sarcolemma leading to muscle contraction. In this process, fibers can stretch, shorten, or remain isometric although producing force. This force, in turn, is transmitted to the tendinous and bony structures [1]. Movement occurs that way. All these forms of motricity work well for a healthy subject. However, everything changes when spinal cord injury (SCI) occurs. **Figure 1** illustrates the central nervous system and its afferent and efferent pathways.

People with SCI have ruptured or impaired communication between CNS and organs that control motor and/or sensory functions. Nerve impulses are electrochemical processes and their transmissions occur in two directions. From CNS to PNS, they trigger muscle contraction processes. From PNS to CNS, they send sensorial processes that capture the stimuli from the surrounding environment as shown in **Figure 1** [1].

SCI harms the neurological responses according to the compromised site, that is, the level of the affected pathways. Thus, a complete SCI, which interrupts all nerve pathways, comprises in the acute-phase (also known as a medullary shock) flaccid paralysis with deep areflexia and muscle hypotonia to, consequently, give rise to spastic paralysis with hypertonia, deep hyperreflexia, and a sign of pyramidal release. Sensitive changes (hypoesthesia or anesthesia) occur for all forms of sensitivity below the level of injury. Partial or incomplete lesions are a consequence of the affected pathways. For instance, if there is a spinal hemisection, then there will be homolateral and contralateral signs and symptoms. On the same side of the injury, paresis or paralysis of the first neuron, abolition of deep sensations and alteration of gait occur. On the contralateral side, thermal and painful anesthesia is observed with no change in strength.

In the last decades, neuroscientists and rehabilitation engineers have been seeking alternatives to recover the mobility of people with SCI. The goal was to provide them with a better quality of life and functional independence. In 2012, the World Health Organization (WHO) asserted that about 0.5% of the population in developing countries needs prosthetic and orthotic devices and that 1.0% of that population needs wheelchairs [3]. Between 250,000 and 500,000 people suffer from SCI in the world, of which the majority are men and women between the ages of 15 and 25 and the elderly over 60 [4]. For the elderly, according to the United Nations Population Report [5], there will be an abrupt increase of people over 60 in 2050, reaching around 1 billion people among healthy individuals, people with SCI, heart

**29**

**Figure 1.**

impacts caused by immobility.

*Central nervous system and its afferent and efferent pathways [2].*

*Hybrid Neuroprosthesis for Lower Limbs DOI: http://dx.doi.org/10.5772/intechopen.83793*

disease, and other factors that may compromise locomotion. More than 1.2 million people in the United States have SCI that disables mobility, generating an estimated annual cost of \$ 40.5 billion [6]. A Canadian study with 1716 individuals with SCI indicated a median lifetime expenditure of \$ 336,000 per person, up to \$ 479,000 if bedsores occur early in the hospital [7]. As costs are high, new techniques and devices are researched and evaluated to reduce these costs and/or minimize the

Devices such as wheelchairs, crutches, and walkers have been in use to aid the locomotion and rehabilitation of the elderly or people with SCI. However, these solutions are not fully effective and users expend great energy. It also requires the assistance of physiotherapists, caregivers, or family members [8, 9]. Therefore, alternatives that reduce the physical demands of users, therapists, and caregivers have been sought. Orthoses, neuroprostheses, and exoskeletons emerged as

*Hybrid Neuroprosthesis for Lower Limbs DOI: http://dx.doi.org/10.5772/intechopen.83793*

*Prosthesis*

ebellar origins.

shown in **Figure 1** [1].

observed with no change in strength.

represents only a few spinal reflexes.

pre-motor, and subthalamic nuclei. There are several paths such as rubrospinal, reticulospinal, vestibulospinal, and cephalospinal paths. The extrapyramidal system and its pathways harmonize the voluntary motor system, guarantee the automatic motricity, and control the postural reflexes of spinal and vestibulocer-

Reflex motricity depends on the pyramidal and extrapyramidal systems and

The CNS triggers nerve impulses that travel along the motor neuron toward the muscle fiber so that contraction can happen. They can excite the neuronal membrane to reach depolarization voltage levels above a triggering threshold that generates a particular wave known as action potential (AP). The AP consistently propagates along the axon toward the synaptic ending. At the synaptic cleft, vesicles deliver the neurotransmitter acetylcholine that connects to cholinergic receptors and depolarizes the myoneural junction. Eventually, the depolarization can generate a new AP that propagates along the sarcolemma leading to muscle contraction. In this process, fibers can stretch, shorten, or remain isometric although producing force. This force, in turn, is transmitted to the tendinous and bony structures [1]. Movement occurs that way. All these forms of motricity work well for a healthy subject. However, everything changes when spinal cord injury (SCI) occurs. **Figure 1** illustrates the central nervous system and its afferent and efferent pathways.

People with SCI have ruptured or impaired communication between CNS and organs that control motor and/or sensory functions. Nerve impulses are electrochemical processes and their transmissions occur in two directions. From CNS to PNS, they trigger muscle contraction processes. From PNS to CNS, they send sensorial processes that capture the stimuli from the surrounding environment as

SCI harms the neurological responses according to the compromised site, that is, the level of the affected pathways. Thus, a complete SCI, which interrupts all nerve pathways, comprises in the acute-phase (also known as a medullary shock) flaccid paralysis with deep areflexia and muscle hypotonia to, consequently, give rise to spastic paralysis with hypertonia, deep hyperreflexia, and a sign of pyramidal release. Sensitive changes (hypoesthesia or anesthesia) occur for all forms of sensitivity below the level of injury. Partial or incomplete lesions are a consequence of the affected pathways. For instance, if there is a spinal hemisection, then there will be homolateral and contralateral signs and symptoms. On the same side of the injury, paresis or paralysis of the first neuron, abolition of deep sensations and alteration of gait occur. On the contralateral side, thermal and painful anesthesia is

In the last decades, neuroscientists and rehabilitation engineers have been seeking alternatives to recover the mobility of people with SCI. The goal was to provide them with a better quality of life and functional independence. In 2012, the World Health Organization (WHO) asserted that about 0.5% of the population in developing countries needs prosthetic and orthotic devices and that 1.0% of that population needs wheelchairs [3]. Between 250,000 and 500,000 people suffer from SCI in the world, of which the majority are men and women between the ages of 15 and 25 and the elderly over 60 [4]. For the elderly, according to the United Nations Population Report [5], there will be an abrupt increase of people over 60 in 2050, reaching around 1 billion people among healthy individuals, people with SCI, heart

central nervous system (CNS) about the level of muscle contraction.

Peripheral motor neurons are part of the peripheral nervous system (PNS) and are organized into motor units. Nerve fibers protract from the anterior roots of the spinal cord to muscle fibers and organs of muscular proprioception called muscle spindles. The spindles send sensorial signals to the spinal cord, informing the

**28**

**Figure 1.** *Central nervous system and its afferent and efferent pathways [2].*

disease, and other factors that may compromise locomotion. More than 1.2 million people in the United States have SCI that disables mobility, generating an estimated annual cost of \$ 40.5 billion [6]. A Canadian study with 1716 individuals with SCI indicated a median lifetime expenditure of \$ 336,000 per person, up to \$ 479,000 if bedsores occur early in the hospital [7]. As costs are high, new techniques and devices are researched and evaluated to reduce these costs and/or minimize the impacts caused by immobility.

Devices such as wheelchairs, crutches, and walkers have been in use to aid the locomotion and rehabilitation of the elderly or people with SCI. However, these solutions are not fully effective and users expend great energy. It also requires the assistance of physiotherapists, caregivers, or family members [8, 9]. Therefore, alternatives that reduce the physical demands of users, therapists, and caregivers have been sought. Orthoses, neuroprostheses, and exoskeletons emerged as

technologies that assist the individual's general health and therapeutic rehabilitation. These devices are capable of producing more intense training, quantitative feedback, and better functional results [9, 10].

In the case of people with SCI, the condition may be irreversible, resulting in some type of paresis: partial hemiplegia, paraplegia, or quadriplegia. Orthoses and/or functional electrical stimulation (FES) allow those people to perform ambulation (active orthoses) and/or provide them trunk stability (passive orthoses). Such technologies facilitate their social reintegration, increase self-esteem, and improve the general quality of life. This can be achieved since these solutions induce a decrease in other affections caused by limb paralysis, such as muscular atrophy, which reduces muscle strength and can prevent functional movements from happening [11–13]. Among the other sequelae that may arise as a consequence of SCI, one can mention: respiratory difficulties, intestinal and/or urinary incontinence, loss of sexual functions, deficiency of lymphatic and vascular system, muscle atrophy (which can result in spasticity), pressure ulcers, thrombosis, and bone demineralization [14].
