**2.1 Indications for treatment**

It's demonstrated that burden of care is higher in neurological patients who developed spasticity than that of those without it, in particular regarding treatment costs, quality of life, caregiver burden, and the effects of comorbidities [21]. The treatment of muscle overactivity may be considered when the condition is disabling. Muscle overactivity usually impairs motor command, so this itself justifies the treatment. Moreover, independently from the aetiological context, it contributes to impair patient's function [22]. Nevertheless, not all patients with muscle overactivity need a specific treatment. Treatment in spasticity should be carried out only after rigorous clinical analysis, in order to determine the severity of functional impairment. A multidisciplinary approach is necessary in order to obtain this specific assessment, being different according to patient's clinical condition; it may include variably physician, physical therapist, occupational therapist, nurse, and/or caregiver [22]. In order to obtain an individual, task-oriented therapeutic strategy, it is necessary to analyse a list of personal measurable objectives, which may be different for each patient. The clinical follow-up is required in order to show the benefits as well as adverse events. Muscle spasticity, which usually is responsive to drug treatment, is not the only motor impairment in spastic paresis. It is necessary also that physiotherapy is associated to drug treatment, in order to obtain maximum gain in paresis. For example, stretch programmes can be used to treat soft tissue shortening. Therefore, before treatment, the following three questions must be answered:


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lesions.

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

**2.2 Physical therapy**

**2.3 Oral drugs**

or dantrolene, is not successful, local treatment is allowed [25], such as muscle botulinum toxin (BTX) injection or peripheral neurolytic blockade with alcohol or phenol [26]. Surgery is to be considered as the final treatment option; however, it is rarely used. If the principal aim is to inhibit neurotransmitter activity at one or more sites within the central nervous system, a systemic approach with specific drugs is to be evaluated. Targeted therapy could regard pre- or postsynaptic sites in spinal interneurons (at varying levels of the upper motor neuron pathway), alpha motor neurons, as well as primary sensory afferent neurons. So, the central nervous system is influenced by inhibitory effects of the neurotransmitters [27]. Oral administration needs high drug dose in order to cross the blood–brain barrier; therefore, side effects like dizziness could occur. In order to reduce the probability for these negative effects, it is possible to introduce some drugs directly into the cerebrospinal fluid, for example, by an intrathecal pump. For drugs used peripherally via injection directly to the nerve or muscle, systemic side effects are fewer.

Physiotherapy is the basic treatment for all patients with spasticity [28, 29]. It may help limit muscle contractures and reduce overactivity for a short period. Physiotherapy together with drug treatment is fundamental to obtain the best functional gain, in order to help patients adapt to changes. In all cases, physiotherapy must be considered as complementary to drugs and surgery. In fact, stretching is considered an import goal in a physiotherapy session, as largely demonstrated [30]. Functional electrical stimulation allows spasticity reduction in antagonists of the stimulated muscles. An interesting use of electrical stimulation is the stimulation of hand and finger extensors during prehension training and mixing of overactive flexor inhibition with extensor activation [31]. Finally, it is important to educate patient in self-rehabilitation sessions comprehensive of stretching postures and

Pharmacologic approaches emphasise oral drugs, neuromuscular blocks, and intrathecal agents. Usually, antispastic therapy is initiated with oral drugs, even though adverse side effects are frequently reported as a systematic effect [32]. Treatment decisions on specific pharmacologic approach are influenced by chronicity, severity, and localisation of spasticity. It was demonstrated that pharmacologic treatments are most effective if used early, in order to avoid muscle shortening and contracture development [33]. However, the time to treat is the first problem to resolve, in particular for drugs. Correctly, spasticity treatment is recommended when it induces a significant functional impairment, in particular regarding daily living activities, or clinical disability such as bad posture, motor capacity, or nursing. When spasticity is diffusely distributed above all in lower limbs, often observed as a consequence of spinal lesions, its treatment is firstly indicated, than in cerebral

The general goal of medical treatment is to decrease spinal reflex excitability by reducing the release of excitatory neurotransmitters or by potentiating the activity of inhibitory circuits. In clinical practice it is important to differentiate objectives in giving spasticity drugs. The technical objectives are focused to induce tone reduction, in order to increase range of motion or ameliorating joint position and promote rehabilitative procedures. Nevertheless, we also have functional therapeutic objectives regarding gait improvement, daily living activity, self-care, and spasm and pain reduction. When we evaluate the real effectiveness of different drug

active exercises, eventually assisted by caregivers and/or orthoses.

Pharmacological interventions for spasticity can be divided into two groups: those that act systemically and those that act locally [24] with the locally acting treatments tending to be more invasive, systemically acting drugs used as a first step [24]. If a systematic approach, which includes baclofen, tizanidine,

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

or dantrolene, is not successful, local treatment is allowed [25], such as muscle botulinum toxin (BTX) injection or peripheral neurolytic blockade with alcohol or phenol [26]. Surgery is to be considered as the final treatment option; however, it is rarely used. If the principal aim is to inhibit neurotransmitter activity at one or more sites within the central nervous system, a systemic approach with specific drugs is to be evaluated. Targeted therapy could regard pre- or postsynaptic sites in spinal interneurons (at varying levels of the upper motor neuron pathway), alpha motor neurons, as well as primary sensory afferent neurons. So, the central nervous system is influenced by inhibitory effects of the neurotransmitters [27]. Oral administration needs high drug dose in order to cross the blood–brain barrier; therefore, side effects like dizziness could occur. In order to reduce the probability for these negative effects, it is possible to introduce some drugs directly into the cerebrospinal fluid, for example, by an intrathecal pump. For drugs used peripherally via injection directly to the nerve or muscle, systemic side effects are fewer.
