Dystonia is a heterogeneous group of diseases with important variability in phenomenology and underlying etiology and pathophysiology. Treatment must be individualized according to the symptomatology and needs of a specific patient. Several efficacious treatments to improve the symptoms of dystonia exist, but few treatments for metabolic and other disorders causing dystonia. The most important therapeutic options are described and discussed. Better understanding of the genetics and pathophysiology of dystonia, the progress of deep brain stimulation, and the possibility of physical therapy greatly improved multimodal therapeutic management of the dystonia patient. However, we are far from a cure; we can only rarely eliminate symptoms, with a few exceptions. For successful treatment, we need to consider specific motor and non-motor aspects of dystonia, different from other movement disorders. It is particularly important to understand the possibility and limitation of each therapeutic option in order to propose and combine different treatments according to the needs of a specific patient.

The treatment of tremor is challenging, and therapeutic options are often limited and non-specific. Treatment always has to be individualized, and apart from the objective severity of tremor, significant importance should be given to subjective severity and impact of the tremor on the patient. Supportive non-pharmacologic and non-surgical methods should be incorporated into the treatment regimen. Finally, surgical therapy is proven and effective in several tremor syndromes and should be offered to eligible patients.

Secondary dystonia comprises a group of diverse dystonia syndromes, including hereditary diseases with a clinical phenotype exceeding dystonia as well as acquired dystonia. The first step in the classification of dystonic symptoms should be according to its clinical characteristics – age at onset, body distribution, temporal pattern and associated features. Limb dystonia in adulthood, as well as craniocervical dystonia presentation in childhood and young adolescence, point away from primary dystonia causes. Associated clinical features such as oculomotor disturbances, parkinsonism, cognitive and neuropsychiatric symptoms, and systemic involvement can be instructive for identifying the underlying dystonia syndrome. The diagnostic workup in patients with secondary dystonia depends on the suspected dystonia syndrome and can include laboratory tests in serum and cerebrospinal fluid (CSF), magnetic resonance (MR) imaging, genetic testing, etc. It is important to identify potential treatable causes, e.g., dopa-responsive dystonia, Wilson’s disease, Niemann–Pick Type C, infectious and autoimmune diseases, etc. Symptomatic treatments are also available.

Dystonia, defined as a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both, results in patterned, twisted, and sometimes tremulous movements. When dystonia is the sole manifestation, it is known as primary dystonia. Primary dystonia is an uncommon disorder and includes genetic forms of dystonia as well as idiopathic dystonia. Dystonia can involve one body part, when it is called focal; more than one contiguous body part, when it is known as segmental; or involving the trunk and more than two body parts, when it is called generalized. This chapter reviews primary dystonia: the epidemiology, the current theories of pathophysiology, the clinical description, and available treatments of genetic as well as the various forms of focal dystonia, including blepharospasm, oromandibular dystonia, laryngeal dystonia, cervical dystonia, focal hand dystonia and truncal dystonia.

Visible scars in the face are an important clinical entity, especially in the wake of trauma and cancer surgery. The first phase of wound healing is the inflammatory phase; the second phase of wound healing, the proliferative phase, is characterized by epithelial regeneration and collagen synthesis.

Tension is the overriding factor adversely affecting all phases of wound healing. Repetitive tension leads to inflammation, which in turn causes increased collagen synthesis and deposition of glycosaminoglycans, resulting in prolonged erythema and scar hypertrophy.

Underlying musculature can generate dynamic tension on a healing wound, particularly in the face.

A reduction of secondary tension and movement of the healing scar was achieved with injection of botulinum toxin into the musculature subjacent to the scar. As a result, repetitive movement of the wound edges was minimized, unfavorable effects of repetitive microtrauma on wound healing reduced and healing improved.

Tics are brief, sudden, movements (motor tics) or sounds (phonic tics) that are intermittent but may be repetitive and stereotypic (Jankovic et al., 2022). Although tics often spontaneously improve after childhood, they may persist into adulthood and become associated with a variety of comorbid disorders such as attention deficit disorder and obsessive–compulsive disorder. Tourette’s syndrome (TS), considered a genetic and neurodevelopmental disorder, is the most common cause of chronic tics. Motor and phonic tics consist of either simple or complex movements that may be seemingly goal directed. Motor tics may be rapid (clonic) or more prolonged. Many patients exhibit suggestibility and may have a compulsive component, sometimes perceived as an “urge” or a need to perform the movement or sound repetitively until it feels “just right.” Although tics are often considered relatively benign, many patients with TS have severe or disabling tics. “Whiplash” tics can produce disabling compressive myelopathy, and therefore need to be treated early and aggressively. When oral medications fail to provide satisfactory relief of tics, local chemodenervation with botulinum toxin (BoNT) offers the possibility of relaxing the muscles involved in focal tics without causing undesirable systemic side effects.

Stiff-person syndrome (SPS), formerly termed stiff-man syndrome, is characterized by muscular rigidity and episodic spasms mainly involving the trunk and lower limbs. The typical form is an autoimmune disease characterized by progressive axial rigidity, predominantly involving the paraspinal and abdominal muscles, along with hyperlordosis of the lumbar spine, spontaneous or stimulus sensitive disabling muscle spasms of the abdominal wall, lower extremities and other proximal muscles. Ninety-five percent of patients had GAD-65 and 89% had islet cell antibodies (ICA). A sizeable number of patients also have other antibodies such as those against glycine receptor and glycine transporter 2. SPS associated with neoplasms tends to involve the upper limbs and neck and cranial nerves. Patients with carcinoma of the breast or lung (oat cell carcinoma) may develop SLS with high titers of anti-amphiphysin antibodies. This chapter illustrates the use of botulinum toxin (BoNT) in the treatment of SPS, along with anatomical illustrations demonstrating the typical involved musculature, and approach to injection with botulinum neurotoxin, with tabulated dosing recommendations for the various BoNT formulations.

Breast ptosis is one of the most common conditions treated by plastic surgeons. Inferomedial muscle fibers of the pectoralis major originate on the medial aspect of the sternum and rib cartilage and extend upward and laterally to insert onto the bicipital groove of the humerus. Targeting these fibers with botulinum toxin therefore results in unopposed muscular contraction upwards and toward the shoulder, with consequent elevation of the superior portion of the ptotic breast. Treatment induces breast elevation at one week and persist for 3–4 months.

This chapter details the anatomy of the breast and underlying musculature, using detailed cutaway illustrations, discusses the different degrees of breast ptosis along with patient selection and illustrates the injection sites for botulinum toxin, listing recommended doses for the different toxin preparations. Additional uses for botulinum toxin, including treatment of pectoral muscle spasm, postmastectomy pain syndrome, facilitation of breast reconstruction, pseudo-gynecomastia, and anterior mid-chest wrinkles, are discussed.

Spasticity is part of the upper motor neuron syndrome produced by conditions such as stroke, multiple sclerosis, traumatic brain injury, spinal cord injury or cerebral palsy that affect upper motor neurons or their efferent pathways in the brain or spinal cord. It is characterized by increased muscle tone, exaggerated tendon reflexes, repetitive stretch reflex discharges (clonus) and abnormal spastic posturing. Late sequelae may include contracture, pain, fibrosis and muscle atrophy. The most common pattern of spasticity in the upper limb involves flexion of the fingers, wrist and elbow, adduction with internal rotation at the shoulder and sometimes thumb curling across the palm or fist. The most common pattern of spasticity in the lower limb involves extension at the knee, plantarflexion at the ankle and sometimes inversion of the foot.

Chemodenervation by intramuscular injection of botulinum toxin can reduce spastic muscle tone, normalize limb posture, ameliorate pain, modestly improve motor function and prevent contractures. This chapter uses anatomical illustrations to depict the muscles involved in common patterns of spastic posturing, using a “clinician’s eye” view to demonstrate approaches to injection points, discusses guidance techniques such as electromyography and tabulates dose ranges of the common toxin preparations for specific muscles.

The gingival smile or gummy smile (GS) occurs when more than 2 to 3 mm of gum is exposed. It may be related not only to the excessive elevation of the upper lip by the involved muscles, but also to alterations in anatomical features like lip length, bone and periodontal and dental structures. The amount of exposed gum can largely differ from patient to patient, with some individuals presenting gum exposure of up to 10 mm. This chapter discusses the different subtypes of gummy smile – anterior, posterior, mixed – using detailed anatomical illustrations of each, including the pertinent musculature. A table lists the specific muscles to target for injection in each subtype.

Chronic low back pain (CLPB) is one of the leading causes of physician office visits and work absenteeism in developed countries. Because many of the muscle groups involved in CLBP are easily accessible and respond well to injection, this disorder may be seen as particularly amenable to treatment with botulinum neurotoxin (BoNT). This chapter reviews the pathophysiology, diagnosis and treatment with BoNT of myofascial pain of muscles involved in lumbosciatic conditions (quadratus lumborum, iliopsoas and paravertebral). Physical examination of the patient is discussed and illustrated. Anatomy is reviewed, and anatomical diagrams are provided, along with discussion of guidance techniques, such as fluoroscopy, for the accurate placement and dosing of injections.

Idiopathic cervical dystonia (CD) is characterized by sustained muscle contraction leading to abnormal postures and twisting movements of the head and neck. BoNT is the gold standard for treatment of the abnormal postures and movements associated with CD. It provides a long duration of symptomatic relief of the pain or postures associated with CD with minimal side effects.

The complex regional anatomy in the craniocervical region increases the potential risks of injections in this area. Ultrasound guidance provides useful information about the depth and thickness of the target muscles, structures to be avoided when inserting/advancing a needle, a safe path to the target and the location of the injectate within the muscle. When treating patients with CD, ultrasound is frequently combined with EMG guidance which provides additional information about muscle activity and potential contribution to a posture. This chapter provides a review of ultrasound guidance for injections for craniocervical dystonia

In ophthalmology, botulinum toxin injections are the treatment of choice in essential blepharospasm and hemifacial spasm. However, there are many other indications for botulinum toxin around the eye and orbit, such as several forms of strabismus, especially sixth nerve palsy and vertical strabismus in Graves’ disease, convergence spasm, injection in the lacrimal gland for crocodile tears and lacrimal outflow obstruction, eyelid retraction in thyroid eye disease, protective ptosis in lagophtalmos and corneal wounds and entropion. The injection technique is explained in detail including electromyography (EMG) recordings from the eye muscles and injections in the lacrimal gland and the upper eyelid.

Osteoarthritis (OA) is the most common type of non-inflammatory arthritis that affects the aging population but can present at a younger age in those with trauma or obesity. Inflammatory arthritis (e.g., rheumatoid arthritis [RA] and gout) is characterized by swelling of the joint lining that leads to joint destruction and bony erosions when not optimally treated. The treatment of refractory joint pain remains a big challenge with few available therapeutic options, which include oral analgesics and anti-inflammatories, topical treatments, intra-articular therapies and physical therapy.

Several contraindications and common adverse events limit the long-term use of each medication.

This chapter reviews studies on the use of BoNT-A (onabotulinumtoxinA, ONA) for osteoarticular pain. Supported by pre-clinical laboratory evidence of anti-nociception, intra-articular BoNT seems to be efficacious for knee, shoulder, ankle and tennis elbow joint pain, based on RCT and systematic review data. Injection techniques for these joints are discussed, along with dosing recommendations and clear anatomical illustrations showing injection approach and placement.

Urinary incontinence is a common condition in women. All cases require a basic assessment, while urodynamic studies are indicated in those with complex or refractory symptoms. Initial treatment includes lifestyle advice, behavioural modifications, bladder retraining and pelvic floor muscle training. Synthetic mid-urethral sling procedures have revolutionized stress incontinence surgery and reduced the popularity of ‘traditional’ procedures, such as colposuspensions and pubovaginal slings. With regard to urgency urinary incontinence, antimuscarinic agents are the mainstay of current medical management, while a selective β3-adrenergic receptor agonist (Mirabegron) offers an alternative pharmacological option. Intravesical botulinum toxin and neuromodulation (peripheral or sacral) are available to women with refractory symptoms