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>

In 1980, Alan B Scott published the use of botulinum neurotoxin type A by injection into extraocular muscles for treatment of strabismus. Use in blepharospasm was published in 1985, and cervical dystonia in 1986, followed by hemifacial spasm and other dystonias, including spasmodic dysphonia, hand dystonia, and conditions such as limb spasticity.

Formulations of neurotoxin type A worldwide include: Botox/onabotulinumtoxinA, Dysport/abobotulinumtoxinA, Xeomin/incobotulinumtoxinA, and a Chinese product marketed under various brand names in Asia. Botulinum neurotoxin type B is marketed as Neurobloc/Myobloc, or rimabotulinumtoxinB. PrabotulinumtoxinA and daxibotuinumtoxinA-Ianm are type A toxins under development.

Plantar fasciitis (PF) is the most common cause of chronic heel pain, predominantly impacting those who perform heavy footwork, are avid runners or lare ong-distance walkers. Overuse injury leads to repetitive microtears of the plantar fascia near the calcaneus, irritating pain fibers and producing secondary inflammation. Patients typically have intense heel pain, described as aching, jabbing or burning. Pain usually starts with the first few steps in the morning and is reproduced by palpation of the median tubercle of the calcaneum and with dorsiflexion of the toes.

Conventional treatments such as ice, heel cup orthoses, deep-tissue massage and night splints, periods of immobilization and stretching/strengthening exercise programs can reduce pain satisfactorily. Persistent discomfort may respond to treatments such as ultrasound, iontophoresis and phonophoresis. More severe and recalcitrant cases require extracorporeal shock wave therapy (ECSWT) or local corticosteroid injections. When medical approaches fail, surgery is advocated but can only offer modest results.

This chapter reviews pertinent studies to date on the application of botulinum neurotoxin to plantar fasciitis, and discusses injection technique and dosing, including the WRAMC–Yale technique for injecting the soleus muscle, along with the plantar fascia. Clear anatomical illustrations are provided.

Hyperhidrosis is excessive sweating, beyond physiological needs. It may be divided into generalized and localized/focal types, and into primary/idiopathic and secondary forms. Primary axillary hyperhidrosis appears to be the most frequent type, followed by palmar hyperhidrosis and other patterns. Hyperhidrosis may negatively affect many fields of daily life to a significant extent, including emotional status, personal hygiene, work and productivity, leisure activities and self-esteem.

When injected intra- or subdermally, botulinum neurotoxin (BoNT) blocks the release of acetylcholine from the sympathetic nerve fibers that stimulate the eccrine sweat glands and causes a localized, long-lasting but reversible abolishment of sweating. This chapter describes in detail the techniques for BoNT injection to treat primary axillary and palmar hyperhidrosis, as well as showing treatment of scalp and segmental hyperhidrosis. Techniques for assessing the degree and distribution of hyperhidrosis, the area to be treated and the degree of benefit are described.

Cervical dystonia (CD) is an idiopathic focal dystonia characterized by abnormal head and neck posture caused by tonic involuntary contractions in a set of cervical muscles. Four subtypes, based on the principal direction of posture, consist of:

• - Torticollis: Rotation of the head left or right in the transverse plane.

• - Lateralcollis: Head tilt toward left or right shoulder, in the coronal plane.

• - Anterocollis: Head tilt forward, with neck flexion in the sagittal plane.

• - Retrocollis: Head tilt backward, with neck extension, in the sagittal plane.

The clinical spectrum of CD is extremely variable: the 54 muscles involved in head and neck posture may show complex mixtures of involvement, unilateral or bilateral, with contractions of tonic, tremulous or myoclonic character. Currently, the most effective, and now first-line treatment of CD, has become intramuscular injection of botulinum toxin.

This chapter enumerates the different muscles involved in major subtypes of CD, grouped by anatomical location, and their principal direction of action. Sets of muscles involved in different head postures are presented in tabular format for easy selection and targeting. Dose ranges for individual muscles are tabulated for each of the four commonly used botulinum neurotoxin preparations.