Page 42 - Prosthetic voice rehabilitation-5th edition

3.3 SecondarytreatmentPEsegmenthypertonicity 3.3.1 Introduction Hypertonicity and/or spasm of the constrictor pharyngeus muscles in the pharyngoesophageal (PE) segment are the main causes for failure to acquire fluent tracheoesophageal speech. If patients seem to be troubled by hypertonicity, it is important to confirm this diagnosis. Insufflation through the voice prosthesis into the PE segment using a catheter can give the clinician already a good idea whether the resistance of the PE segment is too high. Insufflation could also be done directly through the TEP after removal of the prosthesis to make sure that the problem is not related to the voice prosthesis itself. Too high resistance can be further objectified through trachea pressure measurement during voicing at a comfortable loudness level. A pressure above 0.4 kPa at that loudness level (approximately 65 dB at 30 cm mouth to microphone distance) indicates hypertonicity. The next diagnostic procedure should be videofluoroscopy, which can differentiate between hypertonicity, stricture, and recurrence.1 Finally, a diagnostic plexus pharyngeus blockade with 1% lidocaine can be carried out, to establish whether a short-term pharmacological relaxation of the constrictor pharyngeus muscles solves the problem temporarily. Literature shows that in some cases, the temporary relaxation helps also long-term to acquire fluent speech.42 The primary mode of treatment of hypertonicity of the PE segment is intensified speech therapy, where the addition of relaxation exercises sometimes can be helpful. Once patients get the feeling for fluency of the air and realize that they should press less strong instead of harder during voicing, conservative speech therapy training might overcome this problem. We reserve the invasive methods, i.e. chemical denervation with Botulinum toxin as the first choice and constrictor pharyngeus myotomy as the second choice, for failures of speech therapy only. 3.3.2 Chemical denervation constrictor musculature with Botulinum toxin 3.3.2.1 Introduction and physiologic effects: Botulinum toxin is an endotoxin produced by the microorganism clostridium botulinum. The disease Botulism is known since the 18th century and the bacteria causing it is isolated in the beginning of the 20th century. The endotoxin blocks the acetylcholine release at the neuromuscular junction and is rapidly (in 30-60 minutes) taken up by contracting muscles. Clinical onset of the symptoms begins in 24-48 hours. The endotoxin causes a permanent denervation of the muscles with atrophy starting after 2 weeks. The nerve endings, however, always regenerate, a process that takes several months. Therefore, the duration of the effect is mostly not more than 3-6 months. Botulinum toxin has a wide range of clinical applications in the head and neck region, such as blepharospasm, cervical and laryngeal dystonia, hemifacial spasm, strabismus, and more recently also for hypertonicity/spasm of the PE segment. Botulinum toxin is commercially available in 2 products: Botox (Allergan) and Dysport (Speywood) (the latter is 4 times less active). The effect is measured in MU (mouse units), where 1 MU = LD50 for Swiss Webster female mice. The LD50 for humans is approximately 2500-3000 MU. The single dose limit is 400 MU, and no serious reactions or adverse events are reported with this dose, but in clinical practice much lower doses are applied. Contraindications are: pregnancy, lactation, 42