**1. Introduction**

According to Lance and colleagues, spasticity is a "…motor disorder characterised by a velocity dependent increase in the tonic stretch reflex with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome…" [1]. Over time, the interest of clinicians on spasticity has increased more and more, topics ranging from pathophysiology to clinical relevance and treatment options [2–8].

However, in everyday management of patients' spasticity symptoms, much more complex situation would be there, full of clinical problems. In fact, other positive and/or negative signs may be observed together with increased muscle tone and deep tendon reflexes. Abnormal cutaneous reflexes, spasms, co-contraction, Babinski reflex, and also dystonia, are described as positive phenomena, and weakness, fatigability, and reduced dexterity are considered negative ones. In clinical practice each problem that we have to treat may have different pathophysiological explanations [9]. A central nervous system lesion determines the upper motor

neuron syndrome, induced by an interruption of descending pathways, which connect the highest centres to the spinal cord. Alternatively, reactivity of spinal cord circuits may be modified by a direct damage, through a different way to elaborate the input from peripheral afferents. It is important to differentiate immediate to delayed consequences of damage to the highest centres in the CNS. The delayed consequences lead to a rearrangement of reactivity in spinal cord circuits, in which it is considered a basis of spasticity. Moreover, spasticity may itself be modified by the consequences of paresis and immobilisation, i.e. development of contractures. Several pathophysiological mechanisms may explain the development of spasticity due to CNS lesions. These mainly include defective inhibition, such as postsynaptic inhibition of alpha motor neurons or presynaptic inhibition of 1a afferents. There is also a defective excitation of inhibitory interneurons underlying reciprocal inhibition, autogenetic inhibition, or recurrent inhibition [10].

Dystonia is defined as a neurological disorder characterised by sustained or intermittent muscle contractions, determining unusual movements and postures or both. Typically dystonic movements are patterned and twisting and may be tremulous. Often, dystonic movements may be started by voluntary action, worsening with typically an overflow muscle activation (Consensus 2013) [11]. Dystonia classification is based on clinical characteristics and aetiology. Indeed, except for hereditary forms, dystonic syndromes may be caused by birth-related or other physical trauma, infection, and poisoning or due to pharmacological treatments, particularly neuroleptics. The clinical characteristics include age at onset, temporal pattern, body distribution, and coexistence of other movement disorders. The etiologic characteristics are the presence or absence of nervous system pathology and the pattern of inheritance [11].

Focal dystonia is a neurologic movement disorder, due to an incorrect sensorimotor modulation, determining involuntary, excessive muscle contractions. Writer's cramp is a specific type of focal dystonia that affects the fingers, hand, or forearm. Writer's cramp is a task-specific dystonia, characterised by hands twisting into odd postures. A specific task induces this sign. Other skilled task-specific movements may induce focal hand dystonia, such as playing a musical instrument, typing, or sewing. Writer's cramp is known also as musician's cramp, focal hand dystonia, arm dystonia, finger dystonia, task-specific dystonia, and occupational cramp or dystonia.

Task-specific dystonia like writer's cramp may appear in anyone. It usually appears between 30 and 50 years of age. Task-specific dystonia, particularly musician's cramp, is more common in men.

Two types of writer's cramp could be described:


Probably, repetitive movements determine a remapping of the brain's sensorimotor areas. Bad posture of the hands while holding a pen or pencil associated with overuse seems to cause simple writer's cramp. Dystonic writer's cramp is less common than simple ones and may represent a symptom of generalised dystonia. In this case, the involuntary movements can appear also during other non-writing tasks, such as using a fork or handwashing. Rarely, writer's cramp could be the early onset of a generalised dystonia, which is associated with the DYT1 gene [12].

**115**

*Spasticity and Dystonia: A Brief Review DOI: http://dx.doi.org/10.5772/intechopen.91780*

execution:

**1.2 Spasticity**

tendon taps.

Principal key points:

• A tonic stretch reflex.

muscle, causing contraction.

alterations. [13].

**1.1 Pathophysiology of spasticity and dystonia syndromes**

tempting to generate force or movement.

new abnormal reflex pathways [8, 9].

Typically, spasticity is considered as a specific "pyramidal" sign; nevertheless, selective lesions of the primary motor cortex or corticospinal tract often induce hypotonia, deficit, or weakness in distal movements, without inducing spasticity [4]. Only the involvement of non-primary motor areas (premotor and supplementary areas) and the corticoreticulospinal fibres together with cortical lesions may induce spasticity. Corticoreticulospinal fibres sends through the dorsolateral reticulospinal tract descending just anteriorly to the corticospinal tract, a massive bilateral inhibitory projection to spinal motor neurons, which are located in the lateral funiculus of the spinal cord. So the fact that a selective lesion of the anterior limb or the genu of the internal capsula predominantly induces spasticity without an evident motor deficit and vice versa can be explained by the different courses of corticoreticular and corticospinal fibres in the internal capsula. Hence, a lesion involving the corticoreticulospinal fibres will lead to a decreased inhibition (or to an increased facilitation) of the spinal cord and ultimately to spasticity [13, 14]. Three fundamental phenomena occur after a lesion to the central motor pathways assigned to motor command

1.*Paresis:* the quantitative lack of command directed to agonist muscles when at-

2.*Soft tissue contracture and contractile muscle property changes:* shortened position induced by immobilisation due to paresis, causing soft tissue and muscle

3.*Muscle overactivity:* as a consequence of corticospinal pathway lesion, which causes loss of motor command, brainstem descending pathways are activated. Most of these brainstem descending pathways tend to be constantly active, as a consequence a constant muscle activity is maintained. Releasing of growth factors locally is induced in the spinal cord level by the lack of regular descending excitation to the lower motor neurons. So these phenomena induce local sprouting from neighbouring interneurons, creating perfect conditions in order to synthetise new abnormal synapse network, leading to the creation of

Among these changes, which gradually develop, spasticity represents the principal sign detectable. A simple definition of spasticity is an *increase in velocitydependent stretch reflexes* [9, 10] which can be evoked at rest by muscle stretch or

• Mediated by type 1a fibre nerve, predominantly in the muscle spindle. Passive muscle stretch induces exciting of muscle spindle, which sends sensory input back to the spinal cord through monosynaptic way principally but also oligoand polysynaptic reflexes, which at the end induce an efferent impulse to the

*Neurostimulation and Neuromodulation in Contemporary Therapeutic Practice*

tion, autogenetic inhibition, or recurrent inhibition [10].

and the pattern of inheritance [11].

cian's cramp, is more common in men.

write.

Two types of writer's cramp could be described:

neuron syndrome, induced by an interruption of descending pathways, which connect the highest centres to the spinal cord. Alternatively, reactivity of spinal cord circuits may be modified by a direct damage, through a different way to elaborate the input from peripheral afferents. It is important to differentiate immediate to delayed consequences of damage to the highest centres in the CNS. The delayed consequences lead to a rearrangement of reactivity in spinal cord circuits, in which it is considered a basis of spasticity. Moreover, spasticity may itself be modified by the consequences of paresis and immobilisation, i.e. development of contractures. Several pathophysiological mechanisms may explain the development of spasticity due to CNS lesions. These mainly include defective inhibition, such as postsynaptic inhibition of alpha motor neurons or presynaptic inhibition of 1a afferents. There is also a defective excitation of inhibitory interneurons underlying reciprocal inhibi-

Dystonia is defined as a neurological disorder characterised by sustained or intermittent muscle contractions, determining unusual movements and postures or both. Typically dystonic movements are patterned and twisting and may be tremulous. Often, dystonic movements may be started by voluntary action, worsening with typically an overflow muscle activation (Consensus 2013) [11]. Dystonia classification is based on clinical characteristics and aetiology. Indeed, except for hereditary forms, dystonic syndromes may be caused by birth-related or other physical trauma, infection, and poisoning or due to pharmacological treatments, particularly neuroleptics. The clinical characteristics include age at onset, temporal pattern, body distribution, and coexistence of other movement disorders. The etiologic characteristics are the presence or absence of nervous system pathology

Focal dystonia is a neurologic movement disorder, due to an incorrect sensorimotor modulation, determining involuntary, excessive muscle contractions. Writer's cramp is a specific type of focal dystonia that affects the fingers, hand, or forearm. Writer's cramp is a task-specific dystonia, characterised by hands twisting into odd postures. A specific task induces this sign. Other skilled task-specific movements may induce focal hand dystonia, such as playing a musical instrument, typing, or sewing. Writer's cramp is known also as musician's cramp, focal hand dystonia, arm dystonia,

finger dystonia, task-specific dystonia, and occupational cramp or dystonia. Task-specific dystonia like writer's cramp may appear in anyone. It usually appears between 30 and 50 years of age. Task-specific dystonia, particularly musi-

1.Simple writer's cramp, which appears only during writing. The abnormal

postures spring up soon after you pick up a pen. So, it only affects the ability to

2.Dystonic writer's cramp appears not only during writing but also during other activities with your hands, like shaving, dressing, or applying makeup.

Probably, repetitive movements determine a remapping of the brain's sensorimotor areas. Bad posture of the hands while holding a pen or pencil associated with overuse seems to cause simple writer's cramp. Dystonic writer's cramp is less common than simple ones and may represent a symptom of generalised dystonia. In this case, the involuntary movements can appear also during other non-writing tasks, such as using a fork or handwashing. Rarely, writer's cramp could be the early

onset of a generalised dystonia, which is associated with the DYT1 gene [12].

**114**
