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.

Spasmodic dysphonia is a focal dystonia characterized by task-specific, action-induced spasm of the vocal cords.

There are three types of spasmodic dysphonia: Adductor spasmodic dysphonia (ADSD) is characterized by a strained-strangled voice quality and intermittent voice stoppage or breaks, resulting in a staccato-like voice, caused by overadduction of the vocal folds.

Abductor spasmodic dysphonia (ABSD) is characterized by intermittent breathy breaks and associated with prolonged abduction folds during voiceless consonants in speech.

Mixed-type spasmodic dysphonia has features of both.

The efficacy of botulinum neurotoxin (BoNT) injection in the treatment of spasmodic dysphonia has been proven. This chapter enumerates the muscles involved in each type of spasmodic dysphonia, diagrams and describes different approaches for injection, along with the use of guidance techniques such as laryngoscopy and electromyography, and tabulates dose ranges of the different types of BoNT for each muscle.

Botulinum neurotoxin (BoNT) injections are established as a standard procedure for the treatment of muscles in spastic or dystonic children. Superficial and palpable muscles are easy to inject. In contrast, exact needle placement is more difficult and less controllable in deep muscles or those that are small and difficult to selectively identify. Exact needle placement is, however, essential for optimal functional result, avoidance of side effects and evaluation of therapeutic failures. However, clinical application of BoNT without guidance techniques has been shown to be inaccurate. Several techniques are available to guide needle placement for injection. Electromyography is good, but many muscles may be simultaneously active. Electrical stimulation is uncomfortable and painful and often requires anesthesia. CT guidance necessitates exposure to radiation and is costly. By comparison, the advantages of the ultrasound-guided technique are obvious: real-time observation of the injection readily available easily applicable after a manageable learning period cost effective no serious side effects.

This chapter details the use of ultrasound for injection guidance, and discusses indirect and real-time techniques, and both parallel and perpendicular orientations, for needle placement.

Thoracic outlet syndrome (TOS) is a rare, often perplexing disorder caused by compression of neurovascular structures, just above the first rib and behind the clavicle or under the pectoralis minor, leading to cervicogenic–brachial pain and other symptoms in neck and upper limb. This chapter reviews the subtypes of TOS, such as neurogenic and vasogenic, illustrates the anatomy of the thoracic outlet and discusses the common sites of nerve entrapment.

Botulinum neurotoxin (BoNT) is an emerging treatment for TOS. Intramuscular injection of BoNT reduces muscle spasm and produces denervation atrophy of hypertrophied muscles, relieving compression of neurovascular structures and ameliorating both neurogenic and vasogenic symptoms. Risks associated with injection and the BoNT itself make guidance and targeting techniques important. Therefore, ultrasound (US) guidance for accurate injection placement is stressed. This chapter will briefly review TOS and the literature related to use of BoNT for TOS and also provide a detailed review of procedural techniques for US guidance.

Neuropathic pain refers to pain caused by a lesion or disease of the somatosensory nervous system. Diabetic neuropathy, postherpetic neuralgia, radiculopathy pain, trigeminal neuralgia and complex regional pain syndrome are all neuropathic pain syndromes.

Local administration of botulinum neurotoxin (BoNT)) has proven significant effects on the treatment of neuropathic pain. Abnormal muscle contractions contribute to chronic pain. Botulinum neurotoxin serotype A (BoNT-A) is well known to have an effect on inhibition of muscle contraction and this may partially explain its effect on chronic pain. In preclinical models, BoNT-A was found to effectively block the release of several pain-related neurotransmitters, including norepinephrine, substance P, glutamate and calcitonin gene-related peptide, from afferent nerve terminals and dorsal root ganglia. These pain-related neurotransmitters can stimulate depolarization of C fibers, which are responsible for propagation of chronic pain. BoNT-A also decreases local inflammation around the nerve terminal.

This chapter offers clinical description and pictorial illustration for injection of BoNT for the particular conditions of diabetic neuropathy, postherpetic neuralgia and trigeminal neuralgia.

Botulinum neurotoxin (BoNT) is licensed for the treatment of a number of conditions characterized by striated muscle spasticity. However, in recent years, their unlicensed use in the treatment of lower urinary tract conditions has been described (Smith et al., 2004). Chief among these are conditions characterized by detrusor overactivity. Treatment of vulvodynia and chronic pelvic pain, benign prostate hyperplasia (BPH) and detrusor sphincter dyssynergia (DSD) are other emerging indications with promising positive results. This chapter details the use of BoNT for these conditions, giving a clinical definition of each condition, reviewing pertinent studies and describing the injection technique, percutaneous or endoscopic, using anatomical illustrations, and providing dosing recommendations.

In cervical dystonia (CD), outcome of treatment with botulinum neurotoxin (BoNt), is highly dependent on the correct identificationof the muscles involved. There are “simple” (in one plane) and “complex” (in two or more levels) forms of CD. The difficulty lies in the treatment of complex CD, requiring a more extensive analysis. For such analysis, different diagnostic methods are used. These include: ultrasound, CT neck soft tissue imaging (particularly the deep muscles of the neck), electromyography (EMG) of neck muscles, and standardized photographs of patients with measurements of angles (head, neck, thorax).

Cervical dystonia may occur in principle in three axes (rotation, lateral flexion and sagittal flexion). The head or the neck can be affected alone in each of these planes of movements. Therefore, eight clinical forms can be distinguished: torticollis, laterocollis, antecollis, retrocollis, torticaput, laterocaput, antecaput and retrocaput. In this chapter, involved muscles, their origins and insertions are presented in a table for each of these clinical forms. Injection under CT guidance is described.

Oromandibular dystonia (OMD) is a form of focal dystonia that involves the masticatory, lower facial, labial and lingual musculature affected by the trigeminal, facial and hypoglossal cranial nerves. OMD can be classified into various subtypes, which include jaw-opening, jaw-closing, jaw-deviating, lingual, perioral and/or pharyngeal dystonia. Dystonic spasms may result in clenching, or trismus; grinding of the teeth, or bruxism; tongue thrusting; lip pursing; and other movements.

Evidence-based reviews and clinical experience strongly regard botulinum neurotoxin (BoNT) injection as the first-line treatment for OMD. Patients with OMD require careful examination to determine the particular muscles involved and their pattern of contraction to enable proper selection and targeting for BoNT injection. This chapter enumerates the particular muscles involved in each subtype of OMD, discusses localization and approach for injection and use of guidance techniques where applicable, and tabulates typical dose ranges for different formulations of BoNT. Typical adverse events and techniques to avoid them are discussed.

PP> Hemifacial spasm (HFS) consists of involuntary irregular clonic or tonic twitch-like movements of the facial muscles innervated by cranial nerve VII on one side of the face, and is most often a result of vascular compression of the facial nerve at the root exit/entry zone. Non-vascular causes of HFS are less common, and include facial nerve injury, Bell’s palsy, demyelination presumed to involve the facial nucleus and various tumors and space-occupying lesions in the cerebellopontine angle. PP> Twitches usually begin in the periocular region and can progress to the cheek, perioral and platysma muscles. Hemifacial spasm is almost always unilateral. Muscles involved in HFS include the orbicularis oculi, orbicularis oris and zygomaticus predominantly with frontalis, corrugator, nasalis, buccinators, risorius, depressor angularis oris, mentalis and platysma. PP> Injections of botulinum neurotoxin (BoNT) are the preferred treatment of HFS. They are successful in over 90% of patients, with relief lasting approximately 12 weeks, and repeat treatments remaining effective for many years. This chapter lists the pertinent facial muscles along with their principal mechanical actions; illustrates their anatomy under the skin, showing the recommended injection sites; and tabulates the dose ranges of the various toxins in each of the muscles. <COMP: I can’t get rid of the PP coding here without seeming to lose text>

Migraine is a primary headache disorder characterized by enhanced sensitivity of the nervous system associated with a combination of neurological, gastrointestinal and autonomic disturbances (Silberstein, 2004). Chronic headache is a heterogeneous group of headache disorders that include chronic migraine (CM), chronic TTH (CTTH) and other headache types that occur 15 days or more per month (for a minimum of 3 months).

OnatotulinumtoxinA (onabotA) therapy has been used for a variety of disorders associated with painful muscle spasms. It is generally believed that, following intramuscular injection, onabotA produces partial chemical denervation resulting in a reduction in muscle activity and a broader inhibition of peripheral and central pain sensitization. OnabotA therapy is FDA-approved for use in patients with chronic migraine. This chapter discusses the definition of chronic migraine, patient selection for treatment with onabotA, and presents the PREEMPT injection protocol for the application of onabotA, with clinical description and pictural illustration of the injection site.

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.

Botulinum neurotoxin (BoNT) injection is an effective treatment of spasticity in upper and lower limbs. Accuracy of injection needle placement in target muscles is of great importance in maximizing effectiveness of the treatment, and avoiding both treatment failure and adverse events such as weakening of adjacent musculature. Various guidance techniques improve effectiveness and avoid side effects, including anatomical landmark location and palpation, electromyographic guidance, and ultrasound guidance. In recent years, the availability of portable ultrasound devices has facilitated the application of ultrasound guidance, which is quick, painless, and now readily available. This chapter uses photographs, anatomical illustrations, and ultrasound images to illustrate injection techniques for specific muscles involved in the common patterns of spastic posturing.

Various disorders affecting the ears, nose and throat (ENT) are suited for treatment with botulinum neurotoxin (BoNT). This chapter focuses on the following disorders, describing symptomatology, application of BoNT injections, and dosing ranges: laryngeal dystonia, palatal tremor, dysphagia, hypersalivation (sialorrhea), gustatory sweating (Frey’s syndrome), rhinorrhea, hyperlacrimation and speech problems.

Botulinum neurotoxins (BoNTs) are protins derived from the bacterium Clostridium botulinum. Nine serotypes are known; seroptypes A and B have been formulated for clinical use. BoNTs cleave one of the three soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) proteins: vesicle-associated membrane protein (VAMP), synaptosomal-associated protein 25 (SNAP-25), or syntaxin. Upon entry into the synaptic terminal, BoNT inhibits the exocytosis of neurotransmitter containing synaptic vesicles. Cliical effects begin developing within a week after injection into skeletal muscle, then wear off after 2–4 months, requiring repeat injection. Neutralizing antibodies may develop, reducing clinical effects. Newer toxin preparations under development are listed in a table.

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.

Tremor is one of the common movement disorders encountered by neurologists in clinical practice. Based on the history and phenomenology, the tremor can be classified commonly as Parkinson’s disease tremor, essential tremor , essential tremor plus, dystonic tremor, task-specific tremor and other tremor syndromes. This chapter describes the role of botulinum neurotoxin (BoNT) in several tremor conditions and provides some practical clinical pearls related to BoNT injection techniques. Specific muscles involved and the dose range of BoNT are tabulated.

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

Compared with the upper face, the lower face is a less common focus for treatment with botulinum toxin. However, with proper attention to muscular anatomy and function, the results of treatment in this area can be rewarding. Aging skin loses both its elasticity and thickness. These physiologicalchanges, coupled with repeated pleating and contraction of skin, result in rhytids (wrinkles).

In the upper face, relaxing the relevant underlying muscles of facial expression with botulinum neurotoxin (BoNT) injections will eliminate the so-called dynamic rhytids (wrinkles) and, over time, will soften the appearance of static rhytids. In the lower face, the cosmetic effect is less about the elimination of the wrinkles and more about changing appearance, often through paralyzing target muscles to allow unopposed action of complementary musculature. This approach can be useful, for example, to help correct age-related drooping of the nasal tip or the corners of the mouth. This chapter illustrates in detail the anatomy of lower facial muscles and specific injection sites, and discusses injection patterns to achieve specific results.

Blepharospasm is the most frequent cranial dystonia and consists of involuntary, symmetric, tonic or clonic bilateral contractions of the orbicularis oculi muscle, resulting in partial or complete eye closure. Blepharospasm can be primary (idiopathic), secondary or psychogenic. Primary blepharospasm is an adult-onset focal dystonia, manifesting with forceful eyelid closures. Rarely, blepharospasm is secondary to structural brain lesions, drug-induced or other neurodegenerative conditions like atypical parkinsonism. Blepharospasm’s severity may range from increased blinking frequency (only causing minor discomfort) to a persistent and forceful eyelid closure, leading to functional blindness

The orbicularis oculi muscle is the most frequently involved muscle; other involved muscles may include the corrugator supercilii, the procerus and the frontalis. Botulinum neurotoxin (BoNT) is considered the first-line treatment for blepharospasm. Typically, four injections are administered in the orbital or preseptal portion of the orbicularis oculi muscle, but the number of injections can be increased to include the lateral canthus and the pretarsal component of the orbicularis oculi. This chapter diagrams typical injection sites, tabulates dose ranges for different preparations of neurotoxin and lists frequencies of common adverse events.