Craniofacial Pain Neuromusculoskeletal Assessment Treatment and Management

The cranial nervous system: assessment and treatment basics 435 central question in the event of improve- aetiology. To the author’s knowledge, only one ment of a neurodynamic test is whether the pilot study exists that focuses on the cranial patient’s functionality has improved as well. nervous tissue. It concerns benchmark values For example, a patient suffers from tooth- and the reliability of the tests for the mandibu- ache and the dentist is not convinced there lar nerve (von Piekartz 2001). The standardiza- is any inflammation. The neurodynamic tion of neurodynamic tests as presented in test for the mandibular nerve is positive. If, Chapter 17 presents material for discussion in neck flexion, laterotrusion towards the and needs to be evaluated for its (clinical) rel- pain-free side is restricted by comparison evance and ultimately for its reliability and to the affected side, the toothache will be validity. reproduced, and then reduced in extension. Two treatment sessions including active and SUMMARY passive laterotrusion to the symptom-free side with and without upper cervical flexion This chapter gives an overview of current decreases the intensity and frequency of the biomedical understanding of peripheral toothache significantly. The laterotrusion nervous tissue, especially the cranial shows an increased range of motion and nervous tissue. does not reproduce the symptoms any longer. Retrospectively it may be said that The main statements are: the mandibular laterotrusion showed a pos- itive (selective) influence on the mandibular ᭿ There are many anatomical similarities nerve and reduced the neuropathic pain between cranial brain tissues and the (toothache). rest of the peripheral nervous system. The development of ᭿ They both show the same reactions to cranioneurodynamic tests movement. The neurodynamic tests described in Chapter ᭿ Neurodynamic tests for the cranial 17 are based on anatomical knowledge, the lit- nervous tissue are traditionally based on erature, clinical evidence and – where possible the anatomical, biomechanical, clinical – on research results. Current research focuses and – if possible – current research only on the cranial neural tissue in general results. and not so much on its individual movement behaviour. Only anatomical studies confirm ᭿ Knowledge about normal and the probability of intra- and pericranial nerve pathological movement behaviour of entrapments. Case studies frequently claim cranial nervous tissue and the influences that non-diagnosed pain has a neuropathic conservative treatment techniques may have is still insufficient. References Brandt K, Mackinnon S 1997 Microsurgical repair of Barba D, Alksne J F 1984 Success of microvascular peripheral nerves and nerve grafts. In: Aston S J, decompression with and without prior surgical Beasley R W, Thornme C H M (eds) Grabb and therapy for trigeminal neuralgia. Journal of Smith’s plastic surgery, 5th edn. Lippincott-Raven, Neurosurgery 60(1):104 Philadelphia, p 79 Bennet G J 1999 Does a neuroimmune interaction Breig A 1960 Biomechanics of the central nervous contribute to the genesis of painful peripheral system. Almqvist and Wiksell, Stockholm neuropathies? Proceedings of the National Academy of Sciences USA 96:7737 Breig A 1978 Adverse mechanical tension in the central nervous system. Almqvist and Wiksell, Bogduk N 1988 Innervation and pain patterns of the Stockholm cervical spine. In: Grant R (ed.) Physical therapy of the cervical and thoracic spine. Churchill Butler D 2000 The sensitive nervous system. Livingstone, New York, p 1 Noigroup Publications, Adelaide

436 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT Coppietersen M 2001 Physical examination and Gifford L 1998 Neurodynamics. In: Pitt-Brooke J, Reid treatment of neurogenic disorders of the upper H, Lockwood J, Kerr K (eds) Rehabilitation of quadrant – a manual therapeutic perspective. movement: theoretical basis of clinical practice. Thesis, Catholic University, Department of Saunders, London, p 159 Biomedical Sciences, Leuven, Belgium Hall T, Zusman M, Elvey R 1998 Adverse Cornelius C 2002 Erkrankungen der Nerven im mechanical tension in the nervous system? Mund-Kiefer-Gesichts-Bereich. In: Schwenzer N, Analysis of straight leg raise. Manual Therapy Ehrenfeld M (eds) Spezielle Chirurgie. Thieme, 3:140 Stuttgart, p 55 Hasue M 1993 Pain and the nerve root. An Dahlin L B, McLean W G 1986 Effects of graded interdisciplinary approach. Sine 18:2053 experimental compression on slow and fast axonal transport in rabbit vagus nerve. Journal of the Hromada J 1963 On the nerve supply of the Neurological Sciences 72:19 connective tissue of some peripheral nervous system components. Acta Anatomica 55:343 Davies J R 2003 Post dural puncture headache. Anaesthesia 58:398 Hu J W 2001 Neurophysiological mechanisms of head, face and neck pain. In: Vernon H (ed.) The Delcomyn F 1998 Foundations of neurobiology. W H craniocervical syndrome. Butterworth- Freeman, New York Heinemann, Oxford, p 31 Devor M 1994 The pathophysiology of damaged Huck S 2000 Reading statistics and research. Addison nerves. In: Wall P D, Melzack R (eds) Textbook of Wesley Longman, New York pain, 3rd edn. Churchill Livingstone, Edinburgh, p 79 Inoue T, Cohen-Gadol A A, Kraus W E 2003 Low- pressure headaches and spinal cord herniation. Devor M 1996 Pain mechanisms and pain syndromes. Case report. Journal of Neurosurgery 98 In: Campbell J N (ed.) Pain 1996 – an update (1 Suppl):93 review. Course syllabus. IASP Press, Seattle, p 103 Janetta P J 1976 Microsurgical approach to the Devor M, Seltzer Z 1999 Pathophysiology of damaged trigeminal nerve for tic douloureux. In: nerves in relation to chronic pain. In: Wall P D, Krayenbühl H P, Maspes E, Sweet W (eds) Melzack R (eds) Textbook of pain, 4th edn. Progress in neurological surgery, Vol. 7. Karger, Churchill Livingstone, Edinburgh Basel, p 180 Dommisse G F 1994 The blood supply of the spinal Janssen H 2000 Sensibilitätsstörungen nach cord and the consequences of failure. In: Boyling Implantation im Unterkiefer (Eine retrospektive J, Palastanga N, Jull G, Lee D, Grieve G (eds) Studie). Aus der Klinik und Poliklinik für Mund-, Grieve’s modern manual therapy, 2nd edn. Kiefer- und Gesichtschirurgie. Direktor: Professor Churchill Livingstone, Edinburgh Dr. Dr. H. Niederdellmann, Klinik und Poliklinik für Zahn-, Mund- und Kieferkrankheiten der Doursounian L, Alfonso J M, Iba-Zizen M T et al Universität Regensburg 1989 Dynamics of the junction between the medulla and the cervical spinal cord: an in vivo Kleinrensink G J, Stoeckart R, Mulder P G H et al study in the sagittal plane by magnetic resonance 2000 Upper limb tension tests as tools in the imaging. Surgical and Radiologic Anatomy 11:313 diagnosis of nerve and plexus lesions. Clinical Biomechanics 15:9 Dubner R, Sharav Y, Gracely R H, Price D D 1987 Idiopathic trigeminal neuralgia: sensory features Kumar R, Berger R J, Dunsker S B, Keller J T 1996 and pain mechanisms. Pain 31:23 Innervation of the spinal dura: myth or reality? Spine 21:18 Dyck P J, Lais A C, Gianni C et al 1990 Structural alterations of nerve during cuff compression. Lang J 1995 Skull base and related structures. Atlas Proceedings of the National Academy of Sciences of clinical anatomy. Schattauer, Stuttgart USA 87:9828 Lundborg G 1988 Nerve injury and repair. Churchill Elvey B 2001 Peripheres Nervensystem. In: Van den Livingstone, Edinburgh Berg F (ed.) Angewandte Physiologie; Therapie, Training, Tests. Thieme, Stuttgart, p 463 Matheson J W 2000 Research and neurodynamics: is neurodynamics worthy of scientific merit: In: Fields H L, Rowbotham M W 1993 Neuropathic pain: Butler D (ed.) The sensitive nervous system. mechanisms and medical management. 7th World Noigroup Publications, Adelaide, p 342 Congress on Pain. IASP Press, Seattle, p 369 Medeiros F A, Moura F C 2003 Axonal loss after Fromm G H, Sessle B J 1991 Trigeminal neuralgia: traumatic optic neuropathy documented by current concepts regarding pathogenesis and optical coherence tomography. American Journal treatment. Butterworth-Heinemann, Boston, p 1 of Ophthalmology 135:406 Gavilán J, Herranz J, DeSanto L W, Gavilán C 2002 Millesi H 1986 The nerve gap: theory and clinical Rationale and anatomical basis for functional and practice. Hand Clinics 2:651 selective neck dissection. In: Functional and selective neck dissection. Thieme, Stuttgart Mongini F 1999 Headache and facial pain. Thieme, Stuttgart, 2:12

The cranial nervous system: assessment and treatment basics 437 Murzin V E, Goriunov V N 1979 Study of strength of Shacklock M 1995 Neurodynamics. Physiotherapy fixation of dura mater to the cranial bones. 81:9 Zhurnal Voprosy Neirokhirurgii Imeni 4:43 Shacklock M 2005 Clinical neurodynamics. A new Nicholas D S, Weller R O 1988 The fine anatomy of system of musculoskeletal treatment. Elsevier, the human spinal meninges. Journal of Edinburgh Neurosurgery 69:276 Shankland W E 1995 Craniofacial pain syndromes Ochs S, Jersild R A Jr 1984 Calcium localization in that mimic temporomandibular joint disorders. nerve fibers in relation to axoplasmic transport. Annals of the Academy of Medicine, Singapore Neurochemical Research 9(6):823 24:83 Okeson J P 1996 Neuropathic pains: behavior of Sterling M, Jull G, Wright A 2001 The effect of neuropathic pains. In: Bell’s orofacial pains, 5th musculoskeletal pain on motor activity and edn. Quintessence, Chicago, p 403 control. Journal of Pain 2:135 Olmarker K, Blomquist J, Stromber J et al 1995 Sugawara O, Atsuta Y, Iwahara T et al 1996 The Inflammatogenic properties of nucleus pulposus. effects of mechanical compression and hypoxia on Spine 25:665 nerve roots and dorsal root ganglia. Spine 21:2089 Patten J (ed.) 1995 The spinal cord in relation to the Sunderland S 1978 Nerves and nerve injuries, 3rd vertebral column. In: Neurological differential edn. Churchill Livingstone, Edinburgh diagnosis, 2nd edn. Springer, London, p 247 Thomas P K, Olsson Y 1984 Microscopic anatomy and Powell H C, Meyrs R R 1986 Pathology of function of the connective tissue components of experimental nerve compression. Laboratory peripheral nerve. In: Dyck P J, Thomas P K, Investigation 55:91 Lambert E H et al (eds) Peripheral neuropathy, 2nd edn. Saunders, Philadelphia Rappaport Z, Devor M 1994 Trigeminal neuralgia: the role of self-sustaining discharge in the trigeminal von Hagen G 1997 Körperwelten: Einblicke in den ganglion. Pain 56:127 menschlichen Körper. Die Deutsche Bibliothek – CIP Einheitsaufnahme Rossitti S 1993 Biomechanics of the pons-cord tract and its enveloping structures: an overview. Acta von Piekartz H J M (ed.) 2001 Neurodynamik des Neurochirurgica 124(2–4):144–152 kranialen Nervengewebes (Kranioneurodynamik). In: Kraniofaziale Dysfunktionen und Schmerzen. Sauer S K, Bove G M, Averbeck B et al 1999 Rat Untersuchung – Beurteilung – Management. peripheral nerve components release calcitonin Thieme, Stuttgart, p 115 gene-related peptide and prostaglandin E2 in response to noxious stimuli: evidence that the Wagemans P A H M, Velde van de J P, Kuijpers- nervi nervorum are nociceptors. Neuroscience Jagtman A 1988 Sutures and forces: a review. 92:319 American Journal of Orthodontics and Dentofacial Orthopedics 94:129 Schlessel D A, Rowed D W, Nedzelski J M, Feghali J G 1993 Postoperative pain following excision of Waxman S G 2000 The neuron as a dynamic acoustic neuroma by the suboccipital approach. electrogenic machine: modulation of sodium- Observations on possible cause and potential channel expression as a basis for functional amelioration. American Journal of Otology 14:491 plasticity in neurons. Philosophical Transactions of the Royal Society of London 355:199 Schumann D, Hyckel P 2002 Weichteilverletzungen, Verbrennungen und Narben. In: Schwenzer N, Westmoreland B F, Benaroch E E, Daube J R et al Ehrenfeld M (eds) Spezielle Chirurgie. Thieme, 1994 Medical neurosciences, 3rd edn. Little Brown, Stuttgart, p 367 Boston Schwenzer N, Ehrenfeld M (eds) 2002 Plastische und Wilbourn A J, Gilliat R W 1997 Double-crush wiederherstellende Mund-Kiefer-Gesichts- syndrome: a critical analysis. Neurology 49:21 Chirurgie. In: Spezielle Chirurgie. Thieme, Stuttgart, p 403 Wilson-Pauwels L, Akesson E J, Stewart P A, Spacey S D 2002 Cranial nerves in health and disease, 2nd Selvaratnam P, Matyas T, Glasgow E 1994 edn. Decker, London Noninvasive discrimination of brachial plexus involvement in upper limb pain. Spine 19:26 Zakrzewska J M 1995 Trigeminal neuralgia: do we know the cause? Saunders, London, p 40



439 Chapter 17 Assessment and treatment of cranial nervous tissue Harry von Piekartz CHAPTER CONTENTS INTRODUCTION Introduction 439 This chapter gives an overview of the physical examination of cranial nervous tissue. It starts Classification 439 with a short revision of relevant neuroanatomy. Conduction and target tissue tests, palpation Examination of the cranial nervous tissue: and neurodynamic tests are then described in first category 440 detail. The goal is to standardize neurody- namic tests for cranial nervous tissue. The tests Examination of the cranial nervous tissue: are relatively simple to use during examina- second category 446 tion and treatment. Related literature, clinical features and some clinical examples are pro- Examination of the cranial nervous tissue: vided to outline some ways to integrate the third category 494 new material and put theory into practice. For treatment management rationales and pain mechanisms related to cranial nervous tissue, see Chapters 18 and 19. CL A S SIFIC AT ION In the literature, cranial nerves are mostly clas- sified in relation to anatomy, embryology and neurophysiological functions (Wilson-Pauwels et al 2002). In this chapter a classification is suggested which is clinically easy to use during neurodynamic testing. The tests are built on global movements of cranial nervous tissue in order to gain an impression of the tissue dys- function without too much loading on specific tissues. Neurodynamics of cranial nervous tissue can be divided into three main categories:

440 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT ● The first category is the most fundamental, Note: The starting point during all tests is giving the therapist the first clues to cranio- with the therapist positioned at the head of the neurodynamic dysfunction. These tests are plinth and the right cranial nervous tissue is passive neck flexion and neck extension. tested. ● Tests of the cranial nerves which are mostly EXAMINATION OF THE CRANIAL used in the clinic belong to the second cate- NERVOUS TISSUE: FIRST CATEGORY gory. These tests are relatively simple and can be used to screen a broad spectrum of PASSIVE NECK FLEXION (PNF) patients with cranial dysfunction. These are the tests of the trigeminal (V), facial (VII), Introduction accessory (IX) and hypoglossal (XII) nerves. These will be also called the ‘key’ cranial Historically, this test was used to help diag- nerves. nose meningitis (O’Connel 1946). More recently it has also been used for other purposes. ● The other cranial nerves (the third category Neurosurgeons, for example, use passive sus- or ‘particular’ cranial nerves) are less impor- tained neck flexion to alleviate stress on spe- tant but are encountered in certain specific cific intracranial tissue during suboccipital pathologies. The tests are for the olfactory surgery (Doursonian et al 1989). Cadaver (I), optic (II), oculomotor (III), trochlear (IV), studies show what therapists have hypo- abducens (VI), vestibulocochlear (VIII), thesized in practice: that passive neck flexion glossopharyngeal (IX) and vagus (X) moves the meninges in the lumbar spine, as nerves. well as moving and tensing the sciatic tract (Breig 1976, Jannetta 1990). The relationship and the amount of time in the clinic between the different categories are con- The last decade has seen development of sidered in Figure 17.1. In this chapter, cranio- studies on neurodynamics of cranial tissue neurodynamic and conduction tests and the during lateroflexion in addition to other tests palpation of all categories will be discussed. (see Chapter 16). In all cadaver studies and also in clinical computed tomography/mag- First category Neck flexion (NF) netic resonance imaging (CT/MRI) studies Neck extension (NE) (Penning 1968, Doursonian et al 1989), it is clear that upper cervical flexion is specifically Specific clinical responsible for creating marked amounts of patterns, pathology elongation, sliding and compression of the cranial nervous tissue in the dorsal region of Second Third the cranium. In addition, the prepontine and category category premedullary spaces appear to become nar- rower in flexion whereas during extension the Main cranial nerve tests Specific cranial nerve diameter of the spinal cord in the craniocervi- tests cal region is 3–5 mm larger (Breig 1960). Trigeminal (V) Facial (VII) Olfactory (I) Using magnetic resonance imaging, Vestibulocochlear (VIII) Optic (II) Doursonian et al (1989) found in 18 asympto- Accessory (XI) Oculomotor (III) matic subjects that the spinomedullary angle Hypoglossal (XII) Trochlear (IV) from neutral to flexion changes on average 14° Abducens (VI) (range 1–32°) (Fig. 17.2a). Vagus (X) Passive neck flexion is an oft-forgotten Fig. 17.1 Interpretation depends on standard neurodynamic test for examining the tissue. – Clinical patterns musculoskeletal system. For the therapist who – Pain mechanisms sees patients with craniofacial dysfunction and – Reaction to treatment Proposed categories to assess cranial

Assessment and treatment of cranial nervous tissue 441 Fig. 17.2 a Magnetic resonance imaging (MRI) of the cervical spine in neutral and upper cervical flexion. Note the changes at the dorsal side of the brainstem (upper right). b and c Variations of passive neck reflection. a bc pain, this test is extremely important as a basic right hand of the therapist cups around the test before going on to examine cranial nervous occipital bone. The middle and/or ring finger tissue further. of the right hand makes contact with the dorsal part of the parietal bone and the lower arm The neck flexion described here is a stand- rests on the table. The left hand makes contact ard test for detailed examination of the cranial with the maxillary region with the middle and nervous tissue. For the general neurodynamic index fingers under the nose without grasping test related to the musculoskeletal system, see the mandible to make the test more comfort- the work of Butler (2000). able for the patient and to exclude possible unpleasant reactions during the test (Fig. 17.2b). Starting position and method In this starting position the mandible is pre- vented from unnecessary mechanical stress. The patient lies supine, preferably without a An alternative way of testing passive neck pillow but without extension of the head. The flexion, especially in hypersensitive tissue in patient’s arms are by the sides and the legs are this area, is to position the left hand on the together. The patient’s mouth should be slightly forehead (Fig. 17.2c). open so that the masticatory muscles are relaxed and the tip of the tongue is visible. The

442 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT Both hands make a smooth simultaneously nerve. If there are no obvious indications of coupled movement around an artificial axis abnormal changes it is possible to further in the dorsocaudal region of the cranium so monitor lateral deviation by asking the patient that a head-on-neck movement is performed. to put their tongue out, or to apply a spatula to During the passive neck flexion care should be the lateral side of the tongue (see ‘Hypoglossal taken that the patient does not actively assist nerve’, p. 489). the manoeuvre. The fingers placed on the maxilla can guide the patient’s movements in MANDIBLE the required direction, for example lateroflex- ion, rotation or upper cervical flexion, so that The mandible may laterally deviate or even an optimal movement is achieved. Further- protrude during passive neck flexion. This can more, this grip enables the therapist to obtain be an abnormal habit but also an antalgic verbal and non-verbal information. Some of movement adaptation of the mechanical inter- the non-verbal clues to cranial tissue involve- face tissue of the longest branch of the man- ment might concern the eyes, tongue, mandi- dibular nerve, the lingual nerve (Arzouman ble and mimic musculature. et al 1993, Jacobson et al 1998). The therapist needs to be aware of any changes in the tone EYES of the masticatory muscles, especially parts of the temporal and masseter muscles. Correc- ● Widened pupils during the test can indicate tion of the mandibular deviation will often physical dysfunction of cranial tissue in the increase the tone of these masticatory muscles dorsal intracranial region or result from a which means that this deviation is a relevant sympathetic reaction (Butler 2000). protective deformity (Maitland et al 2001, von Piekartz et al 2001). ● Abnormal reactions such as diplopia or extreme deviation of one eye can be FACIAL MUSCLES relevant. It is not uncommon for patients’ facial expres- ● A common pattern of lateralization of one sion to change during neck flexion without this eye – called exotropia (Lang 2000) – is often being painful. Some superficial nerve branches seen in chronic whiplash patients who can in the face can be involved or facial expression exhibit neuropathic changes of the intra- can be a sign of serious intracranial patho- cranial tissue during flexion of the cervical dynamics where the facial nerve is a contribut- spine. In addition, the dura and cervical ing factor (see below for the facial nerve test). spine should be considered as possible sources of abnormal eye position and move- Comment ments (Brown 1995, Gorman 1995a, 1995b). Neck flexion has to be seen as the basic stand- ● Sometimes nystagmus is seen during flexion. ard test not only in a more acute state of tissue It may be necessary to rethink a diagnosis injury but also in chronic ongoing pain states if, on examination, there is strong resistance where relevant physical dysfunction of the or spasm in the neck extensors at the same nervous system is suspected. Once neck flexion time as nystagmus. Benign tumours in the has been tested it is possible to proceed to a middle ear can cause these kinds of symp- specific cranial neurodynamic test, where it toms (Lang 1995). Furthermore it gives a is necessary to add further neurodynamic reason to examine the neurodynamics of manoeuvres (Fig. 17.3). Some variations may the vestibulocochlear nerve for clues that be: suggest an extreme pathology. ● Addition of lower cervical flexion, latero- THE TONGUE flexion or rotation during or at the end of the manoeuvre. Lateral deviation or fasciculation of the tongue during or at the end of the passive neck flexion ● A change in the order of movement, e.g. first can be a relevant sign for possible physical loading in lateroflexion and then in flexion. dysfunction, especially of the hypoglossal

Assessment and treatment of cranial nervous tissue 443 Fig. 17.3 Neck flexion with lower cervical flexion. PASSIVE NECK EXTENSION (PNE) Neck extension is a test that is less of a routine test than neck flexion but can give useful infor- mation (Grant 1988, Butler 1991). The neural and neural-innervated tissue of the dorsal intracranial and upper cervical regions shows a tendency to glide caudally on passive exten- sion (Schlessel et al 1993). Passive extension can be useful as a basic cranial neurodynamic test if extension is observed as a relevant sign during the subjective examination. For example, post-whiplash patients or hemi- plegics (both groups having upper cervical extension) often present. Lower cervical flexion (flexion of the STARTING POSITION AND METHOD cervicothoracic region) can sometimes be very useful to include initially to obtain The starting position is similar to the neck more loading on the cranial nervous tissue. flexion starting position with a change to the This can be especially useful in patients positioning of the hand cupping the occiput with an antalgic forward head posture and the left hand touching the frontal region. where the flexion position provokes the The right forearm is in supination, with the head symptoms. hand cupping the occipitoparietal region. It is ● Addition of standard neurodynamic tests usually more convenient if the treatment plinth for the rest of the body such as straight leg is raised slightly for this manoeuvre and the raising (SLR), the upper limb neurodynamic therapist kneels beside the patient. The neck test (ULNT), or the slump test (Elvey 1986) is then extended from a previously flexed (Case study 1). position. Case study 1 Comment A 26-year-old man presents with tinnitus and Some variations are possible and the same a dull right unilateral facial ache which kind of non-verbal signs may be present. An increases during computer work. His screen awareness of changes in other structures such was on the right side of his desk. as the cervical spine, vertebral artery and the sympathetic ganglions chains is useful here. During testing of the sensitivity of the Structural differentiation related to neck exten- craniofacial structures, neck flexion together sion alone is difficult (Bogduk 1982, Fukui et al with lateroflexion to the left was a little bit 1996). Further tests are required to assess the tight but did not provoke the ‘dull’ ache. possible sources. During slump in neck flexion plus lateroflexion to the left the frequency of the CRANIOCERVICAL DYSTONIA AND tinnitus changed and the dull facial pain THE ASSESSMENT OF PNF AND PNE slowly decreased. The patient avoided upper cervical extension. Neck flexion and extension are often severely restricted or painful in patients with neuro- It is evident from this test that a more logical pathology, and particularly in patients detailed examination of the cranial nervous with craniocervical dystonia. Dystonia is tissue is required using the slump test. not described as a pathology but as a neuro-

444 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT logical syndrome that is recognized by overview of the classification incidence and sustained muscle contraction, repetitive move- gender-specific incidence of CCD. ments and abnormal posture (Fahn 1988). In the last 10 years dystonia in the head and neck CCD is often accompanied by pain which region has been attributed to different diag- is dominantly nociceptive and/or peripheral noses, for example cranial dystonia, cervical neurogenic. This can lead to primary and sec- dystonia, cervical–facial dystonia and otoman- ondary hyperalgesia which can have an effect dibular dystonia (Csala & Deuschl 1994). This on conditioned reflexes of increase of muscle is due to the variety of areas of localization and tone and spasm (Wall & Melzack 1994, Okeson the combination of symptoms. Nowadays the 1995, Ertekin et al 2002). During this increase term is more generalized as a clinical pattern in muscle tone, there is a risk of neuropathies called craniocervical dystonia (CCD) which is of nerves directly contacting these muscles more widely recognized by therapists from because of changes of the neural container. The different disciplines (Jankovic et al 1991, Tarsy occipital, accessory (IX) and the trigeminal 1998). (V) nerves are most frequently involved (Thompson & Carroll 1983, Nook 1985). Some From a neuroscientific approach it is known general features seen in CCD are accompanied that the primary cause of CCD is neurobiologi- by pain during treatment and examination of cal changes in the basal ganglion which might passive neck flexion, extension and latero- be genetic or acquired. Table 17.1 gives a general flexion (Case study 2). Table 17.1 General overview of the classification incidence and gender incidence of craniocervical dystonia Focal dystonias Incidence per Sex ratio million (male:female) Cranial n.i. n.i. Ocular dystonia 5 4:3 Essential blepharospasm n.i. n.i. Mandibular dystonia n.i. n.i. Lingual dystonia n.i. n.i. Pharyngeal dystonia (spasmodic dysphagia) 3 2:2 Spasmodic dystonia (inner laryngeal dystonia) n.i. n.i. Outer laryngeal dystonia 2:9 Cervical 11 3:5 Spasmodic torticollis (cervical dystonia) 8 n.i. Torticollis/retrocollis 2 Laterocollis/anterocollis 1:3 n.i. Segmental dystonias 3 Blepharospasm/oromandibular dystonia (Meige’s syndrome) n.i. n.i. Other combinations of facial and neck dystonias Generalized dystonias n.i. Generalized dystonia with craniocervical symptoms After Casala & Deutschl (1994) n.i., not investigated.

Assessment and treatment of cranial nervous tissue 445 Case study 2 Fig. 17.4 Flexion restriction in a cervical dystonia patient. A 52-year-old female patient had a car accident 5 years ago. She suffered a head injury and was in a coma for 3 weeks. During the rehabilitation period she slowly developed neck stiffness, headaches and started with bruxism and grinding. The neurologist gave her the diagnosis ‘chronic whiplash’. Her clinical pattern of physical examination reflects, in the author’s opinion, the general signs that are seen in patients with CCD: ● During testing her pain was mostly provoked by passive correction. ● During testing spasm of the antagonist was increased (in this case, the deep neck extensors during flexion). ● Hypertrophy of the sternocleidomastoid muscle (Fig. 17.4). ● Upper cervical flexion was restricted and through range passive neck extension and flexion were without pain but with resistance. ● Neck stiffness and headaches were changed during movement. ● Range of active movement was increased and spasm in the masticatory muscles (masseter) was lessened. Why, in some cases, using simple through reflexes resulting from primary or secondary range movement, can the symptoms change hyperalgesia, or by controlled reactions, influ- for a period? It is possible to hypothesize about enced by higher levels such as basal ganglia why a peripheral nociceptive barrage can con- and other brain regions. tribute to dystonia. Therefore passive pain-free movements give ● A long-term nociceptive barrage leads to the patient an opportunity to perceive their spinal motor reflex phenomena in order to environment, past experience, thoughts and protect the involved tissue. The muscle tone feelings and may (in some cases dramatically) increases although there is a minimal load change the clinical patterns of these symp- on the nervous tissue. toms. These phenomena can open new doors for further rehabilitation and management. ● A small amount of afferent information to the nervous system leads to simple motor Once an impression has been gained about patterns (Wall 1999). upper cervical extension and flexion, a clinical choice must be made about the next nerve test. Motor output scenarios are influenced by a The second category tests include: multitude of factors, such as conditioned ● Trigeminal nerve (V) ● Facial nerve (VII)

446 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT ● Glossopharyngeal nerve (IX) nasociliary nerve runs medially through the ● Accessory nerve (IX) medial wall of the orbit via the anterior ethmoid ● Hypoglossal nerve (XII). foramen. As it passes through the foramen, it is renamed the anterior ethmoidal nerve EXAMINATION OF THE CRANIAL (Shankland 2001a) (Fig. 17.5). NERVOUS TISSUE: SECOND CATEGORY Neurodynamic test THE TRIGEMINAL NERVE (V) The cervical spine is moved into upper cervical flexion and left lateroflexion to load the entry Because the trigeminal nerve is the major branches of the trigeminal nerve more in the sensory nerve and one of the largest nerves of brainstem area. The eyes are moved caudally the head region, the functional neuroanatomy for the frontal nerve, medially for the lacrimal is divided into three parts; first the general nerve and laterally for the nasociliary nerve. anatomy is described, followed by detailed Cranial movements can be added (e.g. to the neuroanatomy of the individual branches and frontal bone) which influence the neural con- finally the neurodynamic tests. tainer of the frontal branches. In the orbital region the sphenoid, lacrimal, ethmoid and General anatomy nasofacial bones surround the nasociliary nerve; the zygoma, lacrimal and maxillary The trigeminal nerve emerges on the mid- bones form the bony guides for the lacrimal lateral surface of the pons and has sensory and nerve. motor roots. It runs over a prominence of the petrous temporal bone and forms the sensory STARTING POSITION AND METHOD ganglion (trigeminal ganglion) in the trigemi- nal ‘cave’ in the floor of the middle cranial The patient lies comfortably relaxed in a supine fossa. The trigeminal ‘cave’ is surrounded by position, with the therapist at the head of the the sphenoid, the ventral part of the dorsum patient. The left hand cups around the dorsal sellae of the sella turcica, and parts of the dura. side of the head with the forearm resting on The major divisions of the nerve are the oph- the table. The right hand grasps around the thalmic division (V1), maxillary (V2) and man- laterofrontal side of the head in such a posi- dibular (V3) (Patten 1995, Wilson-Pauwels et al tion that the middle, index and ring fingers 2002). can make contact with the upper, medial and lateral part of the orbit respectively OPHTHALMIC NERVE (V1) (Fig. 17.6a). Relevant functional anatomy The therapist moves the patient’s head into upper cervical flexion and left lateroflexion The ophthalmic nerve is sensory, runs medial using a slight movement of the trunk without to the trochlear nerve (IV) and divides into extra compression of the dorsal side of the three branches before entering the orbital head by the left hand. The right hand guides fissure: the frontal, the lacrimal and the naso- the head movement without putting extra ciliary nerves. pressure on the orbit. The eyeball movement can then be performed using the right index The frontal nerve travels next to the lateral finger which contacts the cranial tip of the section of the orbital fissure of the frontal bone, eyeball. medial to the lacrimal nerve and lateral to the trochlear nerve. The lacrimal nerve reaches the ● By shaft rotation of the index finger the orbit more laterally and runs to the lacrimal eyeball moves caudally (Fig. 17.6b). gland together with the lacrimal artery. The ● For the orbit, the right index finger grasps around the orbital wall and gives small dis- tractions and/or compressions.

Assessment and treatment of cranial nervous tissue 447 Lacrimal nerve Supraorbital nerve Fig. 17.5 Frontal nerve (with lateral and a Ophthalmic nerve. Nasociliary nerve (resected) medial branch) b Nasociliary nerve. Recurrent meningeal branch (tentorial Supratrochlear branch) of the nerve ophthalmic nerve Trigeminal Lacrimal gland ganglion a Ramus communicans (communicating branch) Posterior ethmoid nerve Nasociliary nerve Zygomatic nerve Frontal nerve with (resected) Anterior ethmoid lacrimal nerve nerve Long ciliary nerve Branches to ciliary ganglion (branches providing b sensory innervation of the cornea) End branch to innervate the medial corner of the eye Ciliary ganglion ab Fig. 17.6a–c Neurodynamic test for the ophthalmic c nerve.

448 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT ● For various accessory movements of the duration of testing and treatment must be sphenoid bone, the right thumb contacts based on careful retrospective assessment and the right great wing and the right index reassessment of the patient. finger the left great wing. These can then be moved in different accessory directions (Fig. EYE PAIN AND DYSFUNCTION 17.6c). Manifestations of eye pain and eye dysfunc- ● Accessory movement of the frontal bone tion, such as accommodation dysfunction, such as rotation around different axes as diplopia and minor strabismus, will often described in Chapter 15. present together clinically. Tiredness, post- traumatic neck syndromes or pain elsewhere Palpation in the body may be noted together with these problems. In microsurgical anatomical studies The frontal branches of the ophthalmic nerve of the trigeminal nerve it was reported that the can be palpated in the ophthalmic foramen of ophthalmic nerve leaves the superior orbital the frontal bone (Fig. 17.7). A slight upper fissure. A considerable amount of ophthalmic flexion and contralateral flexion of the head nerve tissue is situated lateral to the cavernous produces more loading for structure differen- sinus and maintains direct contact with the tiation. During palpation in this position, oculomotor and trochlear nerves, and together symptoms are often more severe and occasion- they pass through the superior orbital foramina ally patients will press on this spot to reduce (Umansky & Nathan 1976, Lang 1983, Soeira symptoms. et al 1994, Pareja et al 2002, Tucker & Tarlov 2005). When considering minor cranial neuro- Comment pathies it appears that the narrow mechanical SENSORY DISTRIBUTION interface (orbit and the other nerves) can influ- ence the pathophysiology. For many patients Because of the rich sensory distribution of the who fit into this clinical pattern, neurodynamic ophthalmic division the author must stress the testing and treatment of this nerve, together need for awareness of the possible high level with the oculomotor and trochlear nerves and of nociceptive afferent barrage in the nervous the orbit, are useful. system. This can have a quick normalizing effect in reducing symptoms, but can also MAXILLARY DIVISION (V2) result in a strong disturbance of pain mecha- nisms (Shankland 2001a). The intensity and Relevant functional anatomy Fig. 17.7 Palpation of the ophthalmic nerve in the The maxillary nerve runs directly to the ophthalmic foramen. foramen rotundum of the greater wing of the sphenoid. As it exits the foramen rotundum it gives off several collateral branches (Fig. 17.8): ● The zygomatic nerve: This nerve pierces the frontal process of the zygomatic bone. A second branch, the zygomatic temporal nerve, traverses the lateral part of the orbit. ● The infraorbital nerve: This nerve passes through the infraorbital foramen of the maxilla. ● The palatine nerves: These originate in the hard and soft palate (foramen palatinum) (Shankland 2001b, Wilson-Pauwels et al 2002).

Ramus communicans Assessment and treatment of cranial nervous tissue 449 (communicating branch) Zygomatic nerve Infraorbital canal Infraorbital nerve Ganglion branches Infraorbital foramen Passage through foramen rotundum Trigeminal ganglion Meningeal branch Pterygopalatine ganglion Fig. 17.8 Maxillary nerve. Neurodynamic test caudal eye movement is produced by flexing the right index and middle fingers with the An upper cervical flexion and contralateral palm of the hand over the temple (Fig. 17.9a). lateroflexion load the nerve branches around For accessory movements of the zygomatic the brainstem. Eye movement must be added bone, the right thumb and index finger contact medially and caudally for the zygomatic tem- the zygoma. Intraoral maxilla and palate tech- poral branch of the maxillary nerve. Cranial niques can also be added as described in movement can change the environment from Chapter 15. The therapist moves the elbow the zygomatic facial branches by moving the towards the patient’s front to enable an acces- zygoma. The infraorbital branches are influ- sory movement of the zygoma, maxilla and enced by maxillary movements and the palate palate. To test the palate the most general does the same for the palatine branches. approach is via longitudinal cranial move- ments (Fig. 17.9b) and for the zygoma and STARTING POSITION AND METHOD maxilla rotation around the transverse axis. The patient lies supine and is comfortable and Palpation relaxed. The therapist sits beside the patient’s head, holding the head with the left hand. The The infraorbital area is easy to palpate at the right index and middle fingers are positioned infraorbital foramen (Fig. 17.10). Find the nerve on the lateral side of the eyeball while the palm with the most resistance and twang back and of the right hand makes contact with the tem- forth as if it were a guitar string. Use the same poral bone region. Contact with the zygoma, principles for the zygomatic branches on the maxilla and palate is possible using the same frontal process. ‘Loading’ the nerve more by technique, so that passive movement of these upper cervical flexion and contralateral eye areas can be performed easily. movement can change symptoms during palpation and might be a valuable source of The therapist moves the patient’s head using information. a slight trunk movement in upper cervical flexion and contralateral flexion. A medial

450 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT a Fig. 17.10 Palpation of the maxillary branches around the intraorbital foramen. b Fig. 17.11 Infraorbital scar tissue and bony changes following a maxillary fracture (reproduced with Fig. 17.9 Neurodynamic test of the maxillary permission from Lang 2000). division. tight around the infraorbital, nasal rami and Comment ethmoidal branches. Subjective signs such as hyperalgesia and sharp pain in the nasal eye TRAUMA IN THE ORBITAL REGION region and maxilla are often described (Stefan 1994, Shankland 2001a, Schwartz-Arad et al Signs and symptoms which can be changed by 2004). Wearing tightly fitting diving goggles neurodynamic testing in this region are often can lead to pathomechanical changes in the seen in post-traumatic disorders such as frac- supraorbital and supratrochlear nerves and tures of the infraorbital wall or superior wall may bring on neuralgia. Using a stethoscope of the maxillary sinus (Fig. 17.11). Developmen- can often lead to neuropathy in the region of tal and growth abnormalities of the palate the auricularis magnus nerve when the stetho- such as tooth-related problems (toothache scope is worn around the neck for a long time. without tooth decay), maxillary sinusitis and Reddy et al (1987) and others describe that abnormal signs may be reproduced by other after approximately 10 minutes of compression neurodynamic tests from the extremities such of the nerve by the stethoscope, symptoms as ULNT, SLR or slump. MINOR ENTRAPMENTS OF OPHTHALMIC AND MAXILLARY BRANCHES The ‘pair of glasses’ syndrome describes the effect of wearing glasses that are too heavy or

Assessment and treatment of cranial nervous tissue 451 such as a burning feeling or pins and needles STARTING POSITION AND METHOD can develop (Costen 1934, Shankland 1995). The patient lies comfortably relaxed in a supine MANDIBULAR DIVISION (V3) position with the head over the plinth, with the hands on the abdomen. The therapist Relevant functional anatomy grasps with both hands around the occiput region. Both thumbs are on the angle of The mandibular nerve (V3) travels laterally the mandible and the therapist’s stomach sup- from the trigeminal ganglion through the ports the patient’s head without compression foramen ovale, which is a hole approximately (Fig. 17.13a). The patient has to relax the man- 1 cm in diameter and 2–3 mm in length located dible. The patient is asked to bring the tip of in the greater wing of the sphenoid (Fig. 17.12). the tongue against the palate with a small Because of the variety of branches it gives off mouth opening, followed by relaxing the as it exits, different neurodynamic loading is tongue back again into the floor of the possible. mouth, whereby the mandible stays in this position (a mouth opening from an average ● Buccal nerve: A motor branch of the man- of 1.5 cm measured from the upper to the dibular nerve, the buccal nerve runs a deep lower incisors). course through the cheek to the masseter and pierces the lateral pterygoid muscle. For the upper cervical spine a head-on-neck movement of the patient (Fig. 17.13b) is made ● Lingual nerve: This nerve runs downwards about an imaginary transverse axis which along the mandible from the trigeminal runs through the first two vertebrae. The ganglion, through the lateral pterygoid second movement is a lateroflexion of the muscle, then somewhat deeper on the medial upper cervical spine (head-on-neck move- pterygoid muscle, ending in several skin ment), whereby the imaginary sagittal axis branches. also runs between the first and second verte- brae (Fig. 17.13c). The therapist guides both ● Auriculotemporal nerve: A branch of the movements with the hands and performs the mental nerve which runs below the head of movements by a trunk movement in the direc- the mandible to the ventral part of the acous- tion that is being examined. Both movements tic meatus. are performed in maximal permitted resist- ance and/or pain to ensure optimal loading of ● Mental nerve: This nerve enters the man- the intracranial tissue which is necessary for dibular foramen into the mandibular canal the testing of the extracranial branches of the which has a length of approximately 4–6 cm. mandibular nerve. In this position, latero- Within the canal some branches run to the pulsion or lateral shift away (here to the left) lower teeth. The end of the nerve pierces the has to be executed. The patient’s head is held mental foramen. in this combined upper flexion position using the left hand. The right hand moves slowly to Neurodynamic test the right side of the mandible and the right index finger is positioned on the superior part Upper cervical flexion and contralateral latero- of the mandible whereby the metacarpal joint flexion of the cervical spine is the first man- lies under the right corner of the mouth. The oeuvre for changing neurodynamics around right middle finger contacts the mandible the brainstem. Depression (approximately inferiorly so that the right side of the mandible 1.5 cm) and contralateral deviation of the man- is covered by these two fingers. dible are needed for the lingual and mental nerves. For the buccal and auriculotemporal Before the manoeuvre, the therapist should branches transverse movements medially and/ check if the patient’s mouth is still relaxed and or laterally are added. Sphenoid movements the tongue is still on the floor of the mouth. If can influence the foramen ovale through which not, the patient is asked to relax the mandible the mandibular nerve runs.

Tympanic 452 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT nerve Ganglion Gasseri Palatine veli tensor nerve (trigeminal ganglion) Meningeal branch Otic of mandibular ganglion nerve Medial pterygoid Foramen nerve spinosum Anterior deep Superficial Tympanic chord temporal nerve temporal nerve (from cranial nerve VII) Parotid branch Posterior Unseparated auricular trunk nerve Ramus communicans Posterior deep temporal nerve Anterior Posterior trunk trunk Nerve of external Masseteric nerve Lateral pterygoid acoustic meatus nerve Anterior Buccal auricular nerve nerve Ramus communicans Lingual nerve and facial nerve Auriculotemporal nerve Mandibular Submandibular Sublingual nerve foramen ganglion Dental branches Inferior alveolar nerve Incisive nerve Mental nerve Parotid nerve Mylohyoid nerve Fig. 17.12 Mandibular nerve (reproduced with permission from Shankland 2001c).

Assessment and treatment of cranial nervous tissue 453 ab cd Fig. 17.13a–d Neurodynamic test for the mandibular nerve. by taking the tip of the tongue back against the REFERENCE VALUE AND RELIABILITY palate followed by relaxing the tongue on the OF THE NEURODYNAMIC TEST OF floor of the mouth. If this has been checked, THE MANDIBULAR NERVE lateropulsion to the left can be carried out. Be mindful that lateropulsion is a curving, not a The test was undertaken using laterotrusion linear movement. of the mandible in a combined position of craniocervical flexion and lateroflexion to the Lateropulsion is performed by a small body other side. It was performed on 50 volunteers movement without increasing pressure in the (26 asymptomatic and 24 patients with a right hand or underarm (Fig. 17.13d). The qual- whiplash-associated disorder) and the range ities that can be noted are types of resistance, of the laterotrusion, localization, intensity and end-feel, noises, range of movement and symp- quality of the sensory responses were meas- toms that can be reproduced. ured. Some major results were discussed (von Piekartz et al 2001). An alternative method of influencing the neurodynamics is to move the head on the The intraclass correlation coefficient for the mandible, for example a transverse movement intertester reliability of the mandible’s latero- medially or accessory movements of the sphe- trusion in neutral (without flexion and latero- noid bone such as transverse or rotation around flexion of the craniocervical region) was a sagittal axis. 0.72 to the left and 0.79 to the right. In

454 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT neurodynamic position this was 0.77 and 0.90, part of the medial pterygoid muscle. The best respectively, which means that the intertester approach is to relax the soft tissue around the reliability was good to excellent (Haas 1991). mandible using a slight ipsilateral lateroflexion in upper cervical extension and a slight depres- Range of movement of lateropulsion sion of the jaw (approximately 1 cm). In this position the ipsilateral little or ring finger with The range of movement of lateropulsion was supination of the forearm can try to palpate the measured using an electronic calliper between nerve and its branches. Many anomalies have the midline of the upper and lower incisors. been described (Isberg et al 1987). For confir- The extent of lateropulsion with 2 cm mouth mation of the ‘right spot’, the author usually opening was, on average, 22.31 mm (SD ± 2.48) uses a sensitizing movement of the head and to the left, and 22.44 mm to the right (SD ± neck using upper cervical flexion (Fig. 17.14a). 2.37) in asymptomatic probands. This was significantly smaller in the patient group, at INFERIOR ALVEOLAR NERVE 19.88 mm (SD ± 3.55) to the left, and 20.02 mm (SD ± 2.89) to the right. Several small branches run through the mental foramen approximately 1.5 cm laterally from Symptoms and intensity a As with other neurodynamic tests (Kenneally 1985), the proposed neurodynamic test repro- b duced classic sensory reactions: Fig. 17.14 Palpation of the mandibular branches. ● 61.5% (16 of 26 volunteers) experienced a a The lingual nerve. ‘pulling’ feeling no further than the man- b The auriculotemporal nerve. dibular angle, with an average score on the visual analogue scale (VAS) of 1.89 (SD ± 0.45). ● 38.5% (10 of 26 volunteers) informed the examiners of a ‘deep pressure’ in the auriculotemporal region, approximately 1 cm from the middle of the head of the mandible (von Piekartz et al 2001). The score on the VAS was 2.01 (SD ± 0.28). COMMENT The therapist has to interpret these results with caution because of the small group which was tested and because more than just the nervous system was tested (von Piekartz et al 2001). Because the intertester reliability is good, this manoeuvre can be used together with other data collected from the subjective and physical examination for interpretation and decision-making within the therapist’s clinical reasoning processes (Jones et al 2002). Palpation LINGUAL NERVE The lingual nerve is situated on the medial dorsal side of the mandible, up to 1 cm caudal to the head of the mandible on the superior

Assessment and treatment of cranial nervous tissue 455 the midline. Palpation with the index finger is which it will be possible to again test the possible, especially when the patient opens problem area (Patten 1995, Wilson-Pauwels their mouth and the therapist holds the man- et al 2002). dible in lateropulsion to the other side. The therapist can often feel superficial branches on ASSESSMENT OF THE EFFERENTS the palate below the lower incisors. The motor function of the temporal muscles, AURICULOTEMPORAL NERVE masseters and pterygoid and the joint reflex are discussed in the following text. The tip of the index finger is placed 0.5 cm in front of the acoustic meatus and behind the Muscle palpation head of the mandible. With the patient’s mouth slightly open, it is often easy to ‘twang’ this The masseter muscles can be palpated 0.5 cm nerve (Fig. 17.14b). towards the angle of the mandible while the patient clenches the jaw. The muscles can be Conduction tests of the trigeminal compared bilaterally as they stand out as hard nerve lumps. At maximal closure the therapist can hold the tip of the index and middle fingers PURPOSE medially to the lateral jaw line to palpate the distal part of the muscle belly of the medial The purpose of the conduction tests of the pterygoid muscle. trigeminal nerve is to: Sensory function ● Differentiate between a peripheral lesion and a dysfunction in the brainstem The dermatomes should be examined with the patient’s eyes closed. ● Determine whether the motor weakness is uni- or bilateral, and whether of lower or ● Soft touch: This tests large diameter myel- upper motor origin (Spillane 1996) inated nerves. With a camel-hair brush, a small piece of cotton or the tip of a handker- ● Get an idea at which level the target tissue chief, brush the examined area lightly. The needs to be examined or treated. patient should be able to identify softer quality of touch associated with a more ASSESSMENT OF THE AFFERENTS localized area, as well as the direction and Corneal reflex onset of the movement (Fig. 17.15a). The fibres most sensitive to compression or ● Pin prick: This tests small diameter myel- distortion appear to be those fibres responsible inated and non-myelinated nerves. A sterile for the corneal reflex. The earliest sign during needle or a sharp dental explorer is needed a dysfunction but also in pain (e.g. vasomotor for the examination of the head. The ability headaches) is often an impaired or absent to localize the stimulus is recorded as well corneal reflex (Patten 1995, Wagner & Lang as the patient’s assessment of the intensity 2000, Matharu & Goadsby 2003). To assess the in relation to the other side and the rest of corneal reflex, hold the patient’s lower eyelid the body. down as far as possible. It must be the cornea, and not the lids, fluid or even the conjunctiva ● Temperature: This tests small diameter that is stimulated. Have the patient look up as nerves. Take two small pieces of cotton and far as possible and, with a piece of cotton wool place one in a bowl of hot water and the twisted to a point, touch either side of the pupil other in a bowl of iced water. Bring one of (Spillane 1996) to differentiate a problematic the pieces approximately 0.5 cm in front area. Problems might be suspected where the of the face. The patient has to register patient immediately flinches. This can be the decrease or increase in temperature. double checked by testing another area of If unable to do so, a lower or upper the eye where the response is normal, i.e. the motor neurone pathology is hypothesized patient neither flinches nor hesitates, after (Spillane 1996). The therapist needs to be

456 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT a aware that this clinical pattern can be mim- icked by craniomandibular dysfunction in b which an inhibition is noted on examination of the masticatory muscles (Patten 1995). c One way to differentiate is by changing the neurodynamics of the trigeminal nerve or Fig. 17.15 Conduction test of the trigeminal nerve. the upper limbs to determine possible a Testing sensitivity with cotton bud. changes in muscle tone. b Isometric testing of the masticatory muscles. c The jaw jerk test using a reflex hammer. Isometric tests For isometric depression and elevation of the mouth, have the patient place the tip of the tongue against the tip of the palate, opening the mouth just far enough to maintain contact with the palate. In adults this is usually about 2 cm. When this degree of openness is reached, the patient should relax the tongue onto the floor of the mouth. This position allows maximum isometric contraction. For elevation, the therapist takes the patient’s chin between the index and middle fingers of both hands (Fig. 17.15b). For depression, main- tain this position and hold both thumbs under the patient’s chin, asking them to open and close the mouth slowly. After 2–3 seconds of isometric contraction it is possible to test recruitment function by ‘breaking’ the con- traction (Maitland et al 2001, Watanabe & Watanabe 2001, Aizawa et al 2002). Some thera- pists repeat this test three times. If the mastica- tory group tests weak on the right-hand side, the jaw will be easily pushed across to that side when tested (Patten 1995). Spasm and fascicu- lations might also be present. Any or all of these clinical events during break contraction might strengthen the suspicion of conduction dysfunction of the trigeminal nerve. The jaw jerk According to Spillane (1995), the jaw jerk is often sadly ignored by therapists even though it offers a plethora of information about con- duction in the trigeminal nerve. To administer this test, place the left index finger on the patient’s chin while the middle, ring and little fingers rest on the patient’s chest in the vicinity of the sternoclavicular joint. With a percussion hammer, tap downward on the index finger (Fig. 17.15c).

Assessment and treatment of cranial nervous tissue 457 Responses Widespread projection of primary afferents of the first neurone in ● A sudden slight closing of the jaw which the trigeminal brainstem complex can be detected by the palpating finger(s) is (Fields 1990, Sessle 1993) the normal response (Wilson-Pauwels et al 2002). Sometimes, as with other reflexes, no Direct loading of the nerve branches can response is observed. create neurophysiological and neurobiological changes in the caudal nucleus of the trigemi- ● Jaw reflex appears exaggerated and even nal brainstem complex and the possibility of jaw clonus can be found in the event of an convergence with other neurones, for example upper motor neurone lesion above the level from the cervical spine (Hu et al 1981, Okeson of the pons (Fukuyama et al 2000, Aramideh 1995). & Ongerboer de Visser 2002). Ectopic discharges that occur at ● Clonus or a trismus reaction has been seen the sites of nerve injury during facial oral dysfunction after radio- therapy for cancer or for severe pain. These were shown to increase mechanosensi- tivity and chemosensitivity of the nerve as An exaggerated jaw reflex, in combination observed by Devor and colleagues (Devor et al with exaggeration of reflexes in the arms and 1993, Devor 1996). Rappaport and Devor (1994) legs is not necessarily directly related to pathol- note that remyelination of the trigeminal gan- ogy (Spillane 1996). For the therapist it can be glion is the first sign of damage to the rest of used as a reassessment. the trigeminal nerve. This reminds us that we must be alert to the nature of morphological Sometimes it can be useful to perform the changes. Pathophysiological processes such as tests in neurodynamic loading of the cranial the setting up of a circuit between excitatory nervous tissue. A more exaggerated jaw reflex and inhibitory synapses that continues indefi- is seen in cases of undefined cranial facial pain nitely, or so-called autorhythmic firing, starts in upper cervical flexion and lateroflexion in the trigeminal ganglion and sets off the away from the examined side. whole activity, especially in the mandibular division (Connor 1985). Pain or other symp- Table 17.2 gives a general overview of the toms may affect all of the three divisions of the physical examination options for the trigemi- trigeminal nerve. In their study of 8124 patients nal nerve. with craniofacial pain, White and Sweet (1969) noted that 32% had trigeminal nerve Comment involvement with the mandibular nerve dominant and that 17% had mixed distur- MANDIBULAR NERVE PATHOLOGY bances. Zakrzewska and Nally (1988) found that pain was reduced in patients with cranio- Rich variation of sensory branches in facial pain by cryotherapy to the peripheral the craniofacial region and motor innervation nerve branches, particularly the branches of of the masticatory muscles suggest that the mandibular nerve. neuropathies can be influenced by neuro- dynamic changes in the trigeminal nerve. The difference between the functional These include orofacial pain, CMD, tinnitus, anatomy and the neurodynamics of vertigo, eye and ear aches, atypical facial the mandibular nerve branches pain and other neuropathies such as trigemi- nal neuralgia or tic douloureux (Okeson This alone might provide a clue to symptoms 1995, Zakrzewska 1995, Chong & Bajwa 2003). that present in this area. The auriculotemporal, Some examples where dynamic changes in the inferior alveolar and lingual nerves have three nerve might change symptoms from a minor main differences as compared to the other trigeminal neuropathy might include the nerve divisions. following.

458 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT Table 17.2 Overview of the physical examination options for the trigeminal nerve (V) Trigeminal nerve (V) Neurodynamic tests Palpation Conduction tests Ophthalmic division (V1) Craniocervical: Foramen ophthalmicum Upper cervical flexion (supraorbital) Contralatera lateroflexion Craniofacial: Sphenoid Lacrimal Eye movements: Caudal Medial Lateral Maxillary division (V2) Craniocervical: Infraorbital foramen Upper cervical flexion Contralateral lateral flexion Craniofacial: Maxillary Zygoma Sphenoid Palatinum Eye movements: Medial Lateral Mandibular division (V3) Craniocervical: Mandible: Afferents: Upper cervical flexion Angle (lingual Muscle palpation Contralateral nerve) Sensory function: lateroflexion Mental foramen – light touch (inferior alveolar – pin prick Craniofacial: nerve) – temperature Sphenoid Ventral ear (auriculotemporal Efferents: Mandible: nerve) Isometric tests Depression Mandibular reflex Contralateral laterotrusion Transverse head of mandible 1. All three have longer extracranial branches neuropathy (Isberg et al 1987). Another is than the other cranial nerves (Wilson- the case of mandibular growth spurts in Pauwels et al 2002). youth, where the inferior alveolar nerve and the lingual nerve must adapt vertically 2. They have many more extracranial tunnels, and horizontally, respectively (Enlow 1986). anastomoses and fixation points, and thus The intraosseous anterior loop of the infer- must adapt to the resulting dynamic inter- ior alveolar nerve is another oft-forgotten face (Leblanc 1995). A spasm of the ptery- branch where functional neuroanatomy goid medial and pterygoid lateral from a and dynamics might be implicated. It craniomandibular dysfunction is an exam- extends beyond the mental foramen, and ple of how the lingual nerve can influence

Assessment and treatment of cranial nervous tissue 459 anatomical and radiological studies show Hinojosa et al 2003) and aneurysms (Kerber that variations in this branch are relatively et al 1972, Wilson et al 1980). common, with the average length being 6.95 mm and consistent findings of a 2 mm It is not uncommon that in radiographic and loop (Misoh & Crawford 1990, Sadiq et al neurosurgical literature vascular compression 2003). as a possible cause of idiopathic trigeminal 3. The final factor, along with the above ana- neuralgia is observed and described (Jannetta tomical attributes which might realistically 1976, Roberts et al 1979, Sens & Higer 1991, provide some insights into mandibular Ciftci et al 2004). nerve neuropathies, is the enormous range of movement of the craniomandibular joint Retrospectively, good results are seen when to which, at 50–60 mm maximum opening, decompression of the superior cerebellar the mandibular nerve has to adapt (Palla artery, the inferior cerebellar artery or the 1998). basilar artery in the prepontine space or the pontine angle are performed (Jannetta 1976, TRIGEMINAL NEURALGIA Roberts et al 1979, Badwin et al 1991, Sens & Higer 1991). Decompression of the sensory Numerous theories based on clinical and root of the dural sleeve and the motor root also experimental data have been put forward to produce good results (Gardner & Miklos 1959, explain this rare condition of severe paradoxi- Saunders et al 1971, Leblanc 1995). cal pain with a unilateral localization limited to a zone innervated by the trigeminal nerve. On the other hand, several authors have suggested that neurovascular compression is a Attacks of pain are triggered by local stimuli normal anatomical variation and is not respon- to one or more parts of the face or oral or nasal sible for trigeminal neuralgia (Morley 1985, cavity. Sometimes allodynia or hyperalgesia Hamlyn & King 1992). Conditions such as can occur during routine testing with cotton chronic vascularization disturbances and wool or a pin (Gerschman et al 1979, Sweet early denervation may also be contributors 1988, Zakrzewska 1995, Göbel 1997, Wilson- (Sunderland 1948, Hamlyn & King 1992). From Pauwels et al 2002). For detailed classification the literature we can conclude that the patho- of cranial neuropathies, see the Headache physiological and pathomechanical mecha- Classification Committee of the International nisms of the trigeminal nerve in the middle Headache Society (Olesen 1988), the Inter- and posterior cranial fossa are still poorly national Association for the Study of Pain understood (Kerr & Lysak 1964, Gelson et al (Merskey & Bogduk 1994) or others such as the 1994, Robinson et al 2004). Experience, empiri- Maxwell classification (Maxwell 1990). The cal data and clinical evidence from micro- International Headache Society (IHS) has clas- neurosurgery can give the therapist some sified neuralgias into two categories according ideas about how it may be possible to treat to their aetiology: and try to change pathodynamics caused by trigeminal neuralgia (see also Case study 3). ● Neuralgias associated with compression of the nerve root or systemic causes are consid- ● The intracranial blood vessel in the pontine ered ‘symptomatic neuralgias’. angle and mechanical interfaces: Head movement changes the load and contact of ● Neuralgias of unknown cause are called cranial nerves and blood vessels in the ‘idiopathic neuralgias’ (Olesen 1988). pontine angle. Different positions of the head and neck can change the symptoms The most common causes of symptomatic when the pain has a peripheral neurogenic neuralgias described in the literature are character. middle and posterior cranial fossa tumours (Nguyen et al 1986, Bullit et al 1987, Puca ● Type of head movement and position: et al 1995, Barret et al 2002), multiple sclerosis Jannetta (1976) used upper cervical neck plaques (Jannetta 1976, Okeson 1995, Quinones- flexion and Barba and Alksne (1984) used

460 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT Case study 3 a In Figure 17.16a, the 32-year-old patient is b in an unloaded position of the trigeminal nerve tissue (upper cervical extension and Fig. 17.16 Patient with pain from trigeminal tissue. ipsilateral lateroflexion). By loading the right a Position without pain. side (upper cervical flexion and contralateral b Correction of the head to the other side, an on/off lateroflexion) of the head (Fig. 17.16b), tone in the muscles of facial expression as well as pain reaction with burning pain from the right the masticatory muscle increased and the head of mandible to the chin. patient experienced a shooting, stabbing pain in his right cheek and mandible. Pathodynamics of the trigeminal nerve was assumed. Treatment of neurodynamics changed the symptoms of this patient, although the cause remained unclear. The pain started several months after a tooth extraction and there were to date no neurological signs. Management of the trigeminal nerve, passive mobilization of the occipital and sphenoid bones and a home programme reduced his pain by more than 50% on a visual analogue scale. In addition, scores of physical and social functions of the Facial Disability Index showed significant changes after 6 weeks. Before treatment of the trigeminal nerve, this patient had only temporary relief with acupuncture but no other (para)medical treatment. Therapists must ask themselves how many patients with trigeminal neuralgia could be helped with neurodynamic and cranial techniques, including patients with atypical facial pain or with mild symptoms of trigeminal neuralgia (Feinmann 1990, Zakrzewska 1995), who have not been diagnosed as such, but for whom the cause is nevertheless a pathophysiological change such as deafferentation (Loeser 1984), reversed double crush (Upton & McComas 1972) or changed mechanical interfaces (Breig 1976, Leblanc 1995, Butler 2000).

Assessment and treatment of cranial nervous tissue 461 upper cervical lateroflexion to decompress region of the mental foramen where the the blood vessels in the region of the pontine mental nerve exits, etc. angle during surgery. ● Active mobilization of the mandibular ● The cranium as an abnormal mechanical nerve. Movements of the mandible (latero- interface which causes the neuropathy: trusion to the other side) will be assessed in Breig (1976) discovered that 75% of nine different positions of the craniocervical groups of 24 patients with trigeminal region such as upper cervical flexion and neuralgia demonstrated an impingement lateroflexion. phenomenon in the foramen rotundum on ● Target tissue exercises such as mechanical lateroflexion to the contralateral side. and thermal stimuli on the chin and lower Jannetta (1976, 1990), Barba and Alksne lip with a warm and cold cotton wool ball, (1984) and Jannetta and Bissonette (1985) together with functional exercises of the confirmed this during neurosurgical orofacial muscles, will produce an optimal procedures. stimulation of the somatosensory cortex of the orofacial region. INFERIOR ALVEOLAR NERVE NEUROPATHIES FOLLOWING FACIAL NERVE (VII) MANDIBULAR IMPLANTS Relevant functional anatomy The last decade has seen a trend towards mandibular implants posterior to the mental Cranial nerve VII emerges from the brainstem foramen. This has increased the incidence of a dorsolateral to the pons and has four compo- neuropathy of the inferior alveolar nerve in the nents (see Chapter 2) which run laterally and mandibular canal (Zarf & Schmidtt 1990, enter the internal auditory meatus of the tem- Kieser et al 2005). The incidence of postopera- poral bone together with the vestibulocochlear tive reversible hypoaesthesia is in the range of nerve (VIII). This meatus leads to the facial 10–39% and that of irreversible hypoaesthesia canal of the temporal bone which runs later- is between 4 and 19% (Ellies 1992, Janssen ally for approximately 2 cm, then turns 90° 2000). A retrospective study by Janssen (2000) (geniculum), runs posteriorly/inferiorly for found out that in both groups 66% of patients 5 cm and terminates at the stylomastoid in the reversible and irreversible groups were foramen, located behind the base of the styloid moderately to strongly inhibited in general process. A further six branches are formed daily life activities: eating (47%), drinking which run in the facial muscles and are rela- (32%), speaking (55%) and kissing (24%). tively superficial. These branches are the Although these studies could not show whether temporal nerve, the zygomatic nerve, the man- the implants were the cause of the neuropathy, dibular nerve, the buccal nerve, the cervical they do appear to be a concomitant factor for nerve and the posterior auricular nerve (Fig. craniofacial dysfunction and pain. 17.17). Neurodynamic tests (in this case of the Neurodynamic test mandibular nerve), palpation of the nerve branches and conduction tests give the thera- The cervical spine is positioned in upper cervi- pist an impression of the health and sensitivity cal flexion, contralateral lateroflexion and ipsi- of the cranial nervous tissue in this region. lateral rotation to get more load on the branches Depending on what is found, the following directly extracranial which run parallel with clinical decisions may be made: the sternocleidomastoid muscle. ● Careful neural container techniques such as It is possible to influence the auditory meatus active and passive mobilization of the man- and facial canal through temporal bone acces- dible, treatment of the pterygoid lateral and sory movements. Petrosal bone movement medial muscles or skin techniques in the changes the stylomastoid foramen region.

462 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT Branches Temporal branches that innervate Pterygopalatine ganglion the mimic Zygomatic branches muscles Greater petrosal nerve Fig. 17.17 Facial nerve. Outer facial nerve with geniculate ganglion Tympanic chord Stylomastoid foramen Posterior auricular nerve Lingual nerve Parotid gland Buccal branches Mandibular marginal branch Cervical branch Moving the mandible into depression and in contralateral laterotrusion reaches the buccal ramus of the mandibular nerve. Contraction of the ipsilateral mimic musculature creates com- pression tension on the side being investigated. To reach the cervical branch a longitudinal caudal movement of the hyoid bone is used. STARTING POSITION AND METHOD a The patient is comfortable in a relaxed position b lying supine. The therapist sits on the short side of the plinth facing the patient’s head, Fig. 17.18a–e Neurodynamic tests for the facial with both forearms resting on the plinth which nerve. has been adjusted to a convenient height. Both hands cup around the occipital region without extreme compression of the cranium. An alter- native position is to place the left hand on the occipital region and the right hand on the frontal bone when nasal or orbital regions are to be examined or treated. The therapist moves their body minimally with both forearms on the plinth for upper cervical flexion, lateroflexion away and ipsilat- eral rotation of the head (Fig. 17.18a). Movement of the temporal or petrosal bone can be added by moving the right hand in the same position to the lateral side of the head to make contact with the bones as described in Chapter 14 (Fig. 17.18b).

c Assessment and treatment of cranial nervous tissue 463 d For the craniomandibular movement, the right hand grasps around the lateral side of e the mandibular angle, whereby the right index finger lies on the superior part and the middle Fig. 17.18a–e—cont’d finger contacts the inferior part of the chin. In this position it is possible to perform a slight depression and lateral deviation of the mandi- ble to the left to emphasize the mandibular buccal branch (Fig. 17.18c). When hyoid movement is needed, the right index finger and thumb grasp around the hyoid and perform the longitudinal movement towards caudal (Fig. 17.18d). Active movement of the facial muscles by the patient can be initi- ated in any position to change neurodynamics (Fig. 17.18e). Palpation Palpation of the facial nerve is on the one hand easy because it runs relatively superficially and has many branches. On the other hand it is difficult because it has different types of anastomoses (Miehlke et al 1979). Therefore it is essential to be sure that a nerve is being palpated. Twanging of the nerve in different neurodynamic positions often gives a good indication as to whether or not the therapist is on the facial branch. The relatively large extrapetrosal branches of the facial nerve (e.g. the posterior auricular, zygomatic, buccal and mandibular branch) are easily palpable and easy to treat. To ‘preload’, the patient’s head is positioned in slight upper cervical flexion and contralateral lateroflexion and ipsilateral rota- tion. The contralateral hand holds this position by grasping around the top the head. ● Palpating the posterior auricular branch: The tip of the right thumb tries to palpate the ventral side of the petrosal bone from caudal to cranial (Fig. 17.19a). The branch usually lies 5–18 mm on this trajectory in the direction of the external acoustic meatus. The nerve can be followed dorsally on the occipital bone whereby the thumb can remain in the same position. The following nerves can be palpated more easily with the right index or middle finger

464 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT ab cd Fig. 17.19 Palpation of the facial nerve: a Posterior auricular branch; b temporal branch; c buccal branch; d mandibular branch. because they are relatively small and run on a fingers (Fig. 17.19c). When considering treat- hard surface. ment, the one or two finger technique may be chosen, depending on the individual ● The temporal branch can be palpated cranio- anatomy of the patient and/or the desired laterally to the orbicularis oculis muscle effects of the techniques. (lateral from the eyebrow) (Fig. 17.19b). ● The mandibular branch can be palpated ventrally to the parotid gland on the mas- ● Palpation of the zygomatic branch is possi- seter muscle. The masseter muscle can be ble on the superior border of the zygomatic contracted by unilaterally clenching the bone and lateral to the orbicularis oculis teeth, followed by palpation with the index muscle. Anastomoses of the nerve often run and middle fingers in the direction of the through and over the mimic muscles. jaw line. The easiest place to palpate this nerve is on the ventral side of the muscle ● The buccal branch runs under the zygomatic belly (Fig. 17.19d). Once convinced about the bone and over the buccal muscle. Palpation localization of the nerve, the masseter can can be performed by placing a slight pres- be relaxed and the examination continued sure on the nerve against the inferior side of or treatment started. the zygomatic bone and its course followed by light twanging with the index and middle

Assessment and treatment of cranial nervous tissue 465 As various anomalies of the extrapetrosal jective symptoms and the tests of the muscles branches have been described, the therapist of facial expression will change. For example, should be aware that they can never be certain a burning eye pain together with a minor which nerve is being palpated. The therapist closing dysfunction of the eye is respectively needs to make a clinical decision regarding the worse in slight upper cervical extension, ipsi- general physical and subjective characteristics lateral lateroflexion and contralateral rotation. of the nerve as these become apparent during the different manoeuvres. The efferent motor branches of the facial nerve are responsible for the corneal reflex, Conduction tests and are discussed together with the trigeminal nerve. The purpose of the tests is to detect the uni- or bilateral strength of the muscles of facial ASSESSMENT OF TASTE expression, the corneal reflex and to detect changes of taste and secretion. Best discrimination is possible using the four primary tastes, i.e. sweet, salt, sour and bitter. TESTING THE MUSCLES OF FACIAL The tests are carried out with sugar, salt, EXPRESSION vinegar and quinine. The patient sticks out the tongue and closes the eyes and the therapist During the subjective examination the thera- applies the fluid substances on the anterior pist inspects the patient’s face for asymmetry part of the tongue for 2–3 seconds. After each and abnormal movements. To evaluate the test the patient has to swill out the mouth muscles of facial expression the following with water and tells the therapist which of instructions can be given: the primary tastes was perceived. In addition, the activity of the facial muscles has to be 1. ‘Show the teeth’ (Fig. 17.20a): The therapist inspected during the test. notes the symmetry of the nasolabial folds. ASSESSMENT OF SECRETION 2. ‘Open the mouth’ (Fig. 17.20b): The naso- The submandibular and sublingual glands can labial folds are compared. Deviation of be tested by sensory stimulation with lemon the jaw due to craniomandibular dysfunc- tion can overshadow a pseudoweakness of a muscles of facial expression. Fig. 17.20a–e Functions of the facial nerve. 3. ‘Close the eyes, screw them up tightly, then open them again’ (Fig. 17.20c): Assessment of eye muscles. 4. ‘Frown, wrinkle the forehead and raise the eyebrows’ (Fig. 17.20d): Tests the frontal muscle. 5. ‘Show the teeth and open the mouth at the same time’ (Fig. 17.20e): Assessment of platysma. When facial/oral dysfunction is present, tests 1, 3 and 4 are the most appropriate. If the symptoms are due to a neurogenic dysfunction (due to changes of the neural containers, such as compression in the facial canal or swelling of neighbouring muscles) then neurodynamic components of the facial neurodynamic test (especially lateroflexion and rotation), the sub-

466 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT bc d e Fig. 17.20a–e—cont’d sweets or by milking these glands by soft pres- sandy, gritty feeling in the eye. A good impres- sure using the index and middle fingers. Saliva sion can be obtained by placing a small electric secretion is observed at the opening of the duct fan 5–10 cm in front of the patient’s eyes and and the patient detects an increase of fluid in blowing perpendicularly in the open eyes for the mouth. 10–20 seconds. After the test check how the patient is feeling and compare the resultant Lacrimal gland dysfunction commonly secretions left and right by milking the gland presents itself in the form of eye dryness or a

Assessment and treatment of cranial nervous tissue 467 0.5 cm under the eyes. These results should more (Fig. 17.21b). More loading (cervical then be compared with those in neurodynamic flexion, lateroflexion away and rotation towards positions when the therapist considers there to the examined side) gives the same patient less be neurodynamic changes of the peripheral expression. branches of the facial nerve. These neurodynamic principles are useful Table 17.3 gives a general overview of the for treatment by mobilization as well as in- physical examination options for the facial tegration into neurological exercise therapy. nerve. Cranial nerves are richly innervated by their own nerves, termed nervi nervorum, and by Comment the autonomic nervous system that regulates the vascularization of these nerves (Hromada IS NEURODYNAMICS OF THE FACIAL 1963). Changes of the neural container because NERVE USEFUL IN REHABILITATION? of spasm of the mimic muscle due to chronic pain (Kruschinski et al 2003) and neurological Testing in functional positions such as sitting diseases (facial paresis) can change the and standing is more comparative, especially physiological mechanisms of the nerve (patho- for patients with neurological facial paresis. dynamics) and can be a source of symptoms An example of a patient with hemiparesis and (Butler 2000). Alleviating pain and normaliz- facial paresis is given in Figure 17.21. The ing tone of the muscles of facial expression patient has an upper motor neurone lesion using neurodynamic movements can, in the (UMNL). In addition, lower motor neurone author’s opinion, be a reason why the symp- lesion (LMNL) components may play a role in toms of patients with orofacial pain and facial his facial motor dysfunction with regard to paresis can be changed. articulation and eating. In an unloaded posi- tion of the facial nerve (upper cervical exten- HEMIFACIAL SPASM sion, lateroflexion towards and rotation away from the examined side), facial muscle contrac- The IASP describes hemifacial spasm as a tion can be of better quality and the dysfunc- progressive condition which, if not treated, tion therefore reduced (Fig. 17.21a). Palpation characteristically results in unilateral tonic of the buccal nerve stimulates the activity even contraction of the facial muscles. Ipsilateral Table 17.3 Overview of the physical examination options for the facial nerve (VII) Neurodynamic tests Palpation Conduction tests Craniocervical: Temporal ramus Testing of facial muscles Upper cervical flexion Mandibular ramus Assessment of taste Contralateral lateroflexion Posterior auricular ramus Assessment of secretion Buccal ramus Craniofacial: Zygomatic ramus Temporal Petrosal Mandible: Depression Laterotrusion Hyoid: Transverse movements Facial muscles: Tensing Relaxing

468 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT ab Fig. 17.21 Rehabilitation of a patient with facial paresis: a In an unloaded position of the cranial nervous tissue (upper cervical extension, lateroflexion towards the same side and elevation of the shoulder); less inhibition of the facial muscle is seen than in a correct middle position (b). facial weakness is possible (Merskey & Bogduk Slight mechanical stimulation of the vessels 1994). The pain is present ipsilaterally and has around the nerve and the nerve itself evokes the features of trigeminal neuralgia. Most of EMG activity (Howe et al 1977, Oge et al 2005), the patients have compression or distortion such as opening of the dura or the arachnoid of the relevant cranial nerve or abnormal blood decreases EMG activity, probably by the change vessels (Lang & Kessler 1991, Shenouda et al in intracisternal volume and/or pressure on 2005). Microvascular decompression (MVD), the nerves (Møller 1988). From this knowledge mainly in the cerebellopontine angle (Jannetta we learn that the facial nerve and its direct 1970, 1980a, Iwakuma et al 1982, Born 2002), connections such as dura and arachnoid are is the obvious therapy. However, this can extremely mechanosensitive when compro- often be a complication of vestibular nerve mised by abnormal intracranial mechanical injury (Sekiya et al 1991). Spasm and lateral interfaces. Pathophysiological changes such as spread of antidromic activity can be recorded axon plasma flow changes, cross-talk, fibrosis, by electromyographic stimulation (EMS) tech- etc. of the cranial nerves are possible signs that niques during MVD (Møller & Jannetta 1985, the spasm and/or pain are still present 1987). (Zochodne et al 1997).

Assessment and treatment of cranial nervous tissue 469 ! When there is a slow progressive massage and biofeedback (Daniel & Guitar 1978, Boussons & Voisin 1984, Devriese 1986, weakness or spasm on one side of the face Liebenstund 1989, Beurskens et al 1994a, 1994b, it is wise to refer the patient to a specialist Kvale et al 2003). A particularly functional form for further diagnosis. Cranioneurodynamics of rehabilitation, known as ‘mime therapy’, was should be an advance warning here. On the developed by Jan Bronk, a mime actor in other hand, neurodynamics, and in particular Amsterdam (Devriese & Bronk 1977). The neck movement, may make an effective therapy is based on the central theme of mime contribution to changing the pathodynamics and its reciprocity as a concept for positive feel- of the facial nerve and its immediate ings and functional movements (Beurskens et surroundings after surgical decompression al 1994a, 1994b): for hemifacial spasm. To the best of the author’s knowledge, there is no basic ● Typical clinical findings related to cranial literature about investigation and treatment neurodynamics are that, during specific through cranioneurodynamics after facial mime exercises of the face, the patient un- surgery. loads the facial nerve using slight extension, ipsilateral lateroflexion and contralateral PERIPHERAL FACIAL PARESIS rotation. Furthermore, slight elevation of the shoulder and flexion of the ipsilateral arm In Europe, 1 in 5000 people suffers from acute leads to unloading of the neural structures. facial paralysis. For children younger than 10 This is seen more obviously during active years, the frequency is 1 in 20 000 (Verjaal 1955, exercise of the most strongly affected area Miller 1967, Devriese 1986). Patients can suffer as well as during exercises for decreasing from different residual symptoms after a synkinesis. peripheral facial paralysis. These may include reduced activity of the facial muscles, which ● A nice addition to mime therapy and other leads to problems while eating, drinking, speak- exercise methods is to use this unloaded ing and with facial expression, and results in position of the nervous system and espe- further contractures and synkinesis (signs of cially that of the facial nerve together denervation) (Beurskens 1990, Beurskens et al with neurodynamic techniques. This can 1994a, 1994b, Beurskens & Burger-Bots 1995). A have the advantage of changing afferent– rehabilitation programme is indicated when reafferent information and the pathophy- the patient complains about residual symp- siology of the facial nerve (Hromada 1963, toms which do not recover naturally after 1–2 Miehlke et al 1979, Barat 1983, Leduc & years. They can still have considerable synki- Decloedt 1989). One method is to start with nesis, even when the facial nerve has not suf- painless cranioneurodynamics then reas- fered very severe nerve damage (Peitersen & sess the tone and synkinesis and continue Andersen 1966, Mündnich et al 1973, Huffmann with active exercise in the unloaded posi- 1979, Barat 1983, Beurskens et al 1987, von Eck tion to stimulate only the desired facial 1989, Beurskens & Burger-Bots 1995). As litera- activity. If the patient has only mild paraly- ture studies show no consensus about treat- sis in a neutral head position, the therapist ment of facial paralysis patients, no conclusions can add neurodynamic components to make about the outcome can be drawn (Peitersen & the exercise more difficult. Andersen 1966, Huffmann 1979, Beurskens et al 1994a, 1994b, Beurskens & Burger-Bots 1995). ● Local facilitation techniques of the periph- Eighty-five per cent of all studies recommend eral facial branches provide the patient with rehabilitation in the form of exercise therapy, a better circulation, more relaxation of the facial muscles and greater awareness of the face (Liebenstund 1989, Beurskens 1990, Beurskens & Burger-Bots 1995). Another direct technique to influence the tone,

470 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT improve local trophic conditions and facili- clinically (Fig. 17.22). The most frequently used tate the paralysed muscles is local neuro- surgical procedures prescribed for various palpation or neural mobilizations (Butler injuries – otosurgical and parotid operations – & Gifford 1998). Good techniques in the may actually cause damage to the facial nerve. length direction of the different superficial This occurs because nerve anastomoses can branches of the facial nerve are possible and create particularly vulnerable points given can have a positive physiological contribu- the mechanical forces produced at the cross- tion to the local peripheral branches. This section of the junction (Nisch 1973, Breig 1976, can influence peripheral neurogenic symp- Miehlke et al 1979, Hammerschlag et al 1987, toms such as burning pain, inhibition of the Mackinnon & Dellon 1988, Kwan et al 1992, muscle and reduced tone (Woolf & Salter Iriarte Ortabe et al 1993, Butler & Gifford 1998, 2000). Verberne et al 2003). Clinically these clear motor output mecha- Studies of intraoperative electrophysiologi- nisms are often confirmed in the facial cal monitoring of cranial nerves show that the nerve. In cases of long-term facial paresis or facial nerve has a special feature: a small an extracranial pathology, surgery can also amount of traction or compression of the nerve lead to minor dysfunction of the cranial may generate ectopic impulses producing rel- nerves without clear electrodiagnostic change evant detectable EMG discharges from the (Huffmann 1997, Okeson 1995). Examples such facial muscles (Møller & Jannetta 1985, 1986, as capsulitis of the temporomandibular joint, 1987, Harner et al 1986, Armon & Daube 1989, inflammation of the salivary glands, cystec- Nelson & Phillips 1990, Brown & Veitch 1994). tomy in the ear region or symptoms following This could explain the damage that occurs to a blow to the face often cause local trophic the facial nerve during surgery. changes which are easily treatable with neuro- dynamics and local palpation mobilization It is very likely that some minor pathophys- techniques. Perpendicular twang techniques iological changes or neuropathies influence are a good option to treat local signs and symp- signs and symptoms after minor trauma or toms (Butler 1991, Butler & Gifford 1998). In surgery to the face. It is possible to elicit clues addition, facilitation of the paralysed muscle from the patient’s history during subjective group is possible using palpation techniques examination. For example, information about that are simple, cost little time and can easily a ‘spontaneous’ onset of facial pain or dysfunc- be integrated into neuro-orthopaedic concepts. tion might lead to clues that will help the thera- For the different types of facial paralysis, refer pist develop an appropriate treatment strategy. to the specialist literature (Patten 1995). In such cases it is useful to examine the cranial nerves, especially the facial nerve, together FACIAL NERVE ANASTOMOSES with palpation of the facial nerve branches and the anastomosis. Small superficial pain spots Neurosurgeons have long been interested are often found around the anastomosis when in the facial nerve because of its anatomical compared to the other areas. Treatment by variety, particularly in the plexus formation of neural palpation to the anastomosis, together the lateral region of the face (Borucki et al 2002, with neurodynamic facial nerve techniques, Guntinas-Lichius et al 2006). It has been proven can change signs and symptoms dramatically that facial paralysis can be successfully over- in such cases. come with neural repair to part of the hypo- glossal nerve tissue in facial nerve anastomosis. ATYPICAL FACIAL PAIN This results in improved facial muscle func- tion (Miehlke et al 1979). Miehlke and col- Atypical facial pain, which carries the syno- leagues developed a systematic classification nyms of atypical facial neuralgia, idiopathic for the types of anastomoses that are possible facial pain and chronic facial pain, is a persist- ent facial pain that does not have the charac- teristics of the cranial neuralgias, is not

Type I = 48% Temporal branch (T) Type II = 27% Type III = 8% T Type IV = 4% Z Temporofacial part Zygomatic T T Z Z Otomastoid branch (Z) B B foramen Bifurcation M M C Buccal C B M Cervicofacial branches C part Mandibular marginal branch Cervical branch No anastomoses Anastomosis in temporofacial part Anastomosis between temporofacial and Anastomosis (–3) in cervicofacial part cervical part Type V = 5% T Type VI = 3% T Z Type VII = 3% Z Type VIII = 2% Z Assessment and treatment of cranial nervous tissue 471 Z T1 T B 1 1 2 2B 2 B 2B 3 B 1M M M M C C Anastomosis (–1) in cervicofacial part Anastomosis (–1) in temporofacial part C Anastomosis (–2) between temporofacial Anastomosis (–2) in cervicofacial part C and cervicofacial part Anastomosis (–1) in temporofacial part Anastomosis (–1) in temporofacial region Anastomosis (–2) between temporofacial Anastomosis (–2) between temporofacial and cervicofacial part and cervicofacial part Anastomosis (–3) in cervicofacial part Fig. 17.22 Neurosurgical classification for the types of anastomoses of the facial nerve (reproduced with permission from Miehlke et al 1979).

472 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT associated with the physical signs and does not muscles and blood vessels are reported. Man- demonstrate organic causes in the definition agement proposals start with reassurance and put forward by the IHS (Olesen 1988, careful explanation about surgical interven- Zakrzewska 2002). The diagnosis is often used tion (Feinman 1990). Up to half of the patients when the cause is unknown and all terminol- may experience relief of symptoms with re- ogy has been exhausted (Mock et al 1985). assurance together with simple analgesics (Zakrzewska 1995). The characteristic symptoms are pains of different intensity, varying from unilateral Treatment with neurodynamics and cranio- pain to pain affecting the whole face. This dynamics within an overall management is as worsens continually or episodically, is yet not suggested for atypical facial pain as it is enhanced by stress and often connected with for other atypical pain syndromes such as those pain elsewhere in the body (Box 17.1). The most of the shoulder or low back (Butler & Gifford commonly used word from McGill’s pain ques- 1998). Butler and Gifford (1998) and Butler tionnaire is ‘nagging’; ‘shooting’ and ‘sharp’ (2000) recommend general mobilization tech- are used less frequently. This was shown in an niques of the peripheral nervous system com- investigation of 195 patients with facial pain bined with neurodynamic techniques for the (Zakrzewska & Feinmann 1990). This type of facial nerve, as well as pain-free local palpation pain commonly presents with facial arthromy- techniques to change peripheral nociception algia (temporomandibular dysfunction), atypi- and the biochemistry of the central nervous cal dental pain and/or oral dysaesthesia system. In the author’s opinion, this is a good (Harris 1996). On the assumption that the approach. Together with explanation and coop- cause is dental, 75% of patients undergo unnec- eration with other disciplines, therapists may essary dental treatment (Mock et al 1985). make a contribution to the amelioration of these These patients often have a long history of pain symptoms which affect between 25 and 45% of without clear onset and complain of increasing all patients with chronic facial pain (Agerberg pain after craniofacial surgery (Zakrzewska & & Carlsson 1972, Zakrzewska 2002). Feinmann 1990). The physical examination is often unremarkable and without neurological Tinnitus signs (Zakrzewska 1995, Peschen-Rosin 2002). DEFINITION AND PREVALENCE This clinical pattern suggests that deaffer- entation and centralization play an important Tinnitus is a relatively common auditory role in the pathophysiology (Loeser 1984), symptom, defined as the aberrant perception although physical signs such as ‘cramp’ in of sound in the region of the ear and/or head in the absence of an external source of stimula- Box 17.1 Characteristic symptoms of tion (Chan & Reade 1994). In the industrialized atypical facial pain world, the prevalence of constant or temporary tinnitus in adults older than 17 years is 35– ■ Varying severity and character of pain 45%. For those affected, this has a considerable ■ Varies from unilateral to localized to the effect at the activity and participation level. In 0.5% of this group the tinnitus is decompen- whole face sated, i.e. life quality is extremely restricted by ■ Continuous with sharp exacerbations symptoms such as concentration and sleeping ■ Provoked by stress disturbances, reactive depression and fear ■ Relieved by appropriate treatment (Tyeler 2000). ■ Often associated with pain elsewhere in TYPES OF TINNITUS AND EXPLANATION the body MODELS After Zakrzewska (1995). Tinnitus is not a disease, just the ability to hear sounds generated by the auditory (hearing)

Assessment and treatment of cranial nervous tissue 473 Fig. 17.23 A 58-year-old patient who reduces his Articular tinnitus by own manual pressure on his cranium. disc What is the mechanism behind it? External acoustic meatus Stapedius muscle in auditory tube Tympanic velum Tympanic tensor muscle Fig. 17.24 Anatomical connection of the temporomandibular joint and the middle ear. Medioposterior superior fibroelastic tissue part of the joint capsule and the meniscus, attaching onto the neck of the malleus of the middle ear (after Pinto 1962 and designed by Bekkering (2006)). system. This is evidence of compensatory Sicher 1948, 1955, Zimmerman 1959). Recruit- mechanisms that are part of its normal func- ment of the masticatory musculature and tion (Jastreboff & Hazell 2004). Mostly it is clas- muscles in the inner ear also contribute sified as subjective (non-auditory) or objective (Dolowitz et al 1964, Malkin 1987, Hazell et al (clear pathology) tinnitus (Bush 1987, Ganz 1989, 1993). Nerve branches such as the auriculo- Ash & Pinto 1991, Chole & Parker 1992). temporal nerve and the chorda tympani (Costen 1956, Capps 1962, Vernon et al 1992) Subjective tinnitus is the most common and and occlusal abnormalities (Shapiro & Truex disturbing form of the condition (Ganz 1989, 1943, Goodfriend 1947, Kopp 1979, Boero 1989) Chan & Reade 1994). It can be a seriously debil- are also indicated. itating disorder for which a clinical solution may not be available. Different explanations in Embryological correlations (Frumker & Kyle fundamental research and literature suggest 1987, Cohen & Perez 2003) between ear and that subjective tinnitus is more of a functional mandible, also known as otomandibular struc- disorder of the inner ear caused by several tures, are proposed as an important trigger of structures (LePage 1993). tinnitus (Hardell et al 2003). Pinto’s ligament, which is a fibroelastic tissue arising from the Three valid models to explain subjective medioposterior superior part of the temporo- tinnitus are introduced: mandibular joint capsule and the meniscus and attaching onto the neck of the malleus, ● Anatomical/structural is an example of an otomandibular structure ● Neurophysiological (Pinto 1962, Ash & Pinto 1991; Fig. 17.24). ● Cognitive and affective mechanisms. During movement of the jaw this ligament pulls on the malleus which triggers the vesti- Anatomical/structural tinnitus bulocochlear nerve and therefore can change the qualities of the frequency of the tinnitus. Examples of structures responsible are the Stress on this ligament during a cranioman- temporomandibular joint, wear to the roof of dibular dysfunction causes load on the middle the temporomandibular joint socket (Costen 1937) and the eardrum (Shapiro & Truex 1943,

474 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT ear structures and affects the depolarization of larly the brainstem. An excellent literature the vestibulocochlear nerve. This may be why, review about this has been carried out by in some tinnitus patients, protrusion or extreme Levine et al (2003). Tinnitus in the absence of laterotrusion changes the frequency heard. other hearing complaints shares several clini- cal features, such as: Neurovascular compression such as the cere- belli inferior in the posterior fossa (Jannetta ● An associated somatic disorder of the 1980, Meaney 1993, Meansey 1994, Tikkakoski craniofacial and/or craniocervical region 2003) is mentioned (Jannetta 1980b, Meaney et al 1993, Meansey et al 1994, Tikkakoski et al ● Localization of tinnitus to the ear ipsilateral 2003). The middle ear receives its nutrition by to the somatic disorder osmosis and diffusion from the neighbouring blood vessels. This means that a small com- ● No disturbance of balance pression of the main arteries to the middle ear, ● No abnormalities on neurological exami- or changes of the blood vessel tone by auto- nomic dysregulation, can cause an ischaemic nation. situation which influences the function of the stapedial velopalatine muscle which is also In these cases, which are quite common, Levine connected to the middle ear (Xu & Xiong hypothesized the role of the disinhibition of a 1999). brainstem nucleus, the ipsilateral dorsal cochlear nucleus (DCN). Disinhibition of this nucleus Neurophysiological model has consequences for the perception of acous- tic information in the brain which can be inter- The literature can be divided into two parts. preted as tinnitus (Jastreboff et al 1994, Abel & The first has a strong input character, which Levine 2004, Kaltenbach et al 2004). means that nociception of unhealthy tissue from capsule, muscle and peripheral nervous Model of cognitive and affective tissue is directly related to the tinnitus. Here, mechanisms a comparison with facial nerve neuropathy is interesting. For example, abnormal contraction In the last decade, central mechanisms have of the stapedial muscle (which is innervated by been recognized as causes of tinnitus along- the facial nerve) and facial nerve pathology side the traditional medical models. It has been have often been described (Badia et al 1994). shown that emotional and cognitive concepts Watanabe et al (1974) reported eight patients can cause functional impairments that are with tinnitus who could influence it by facial related to tinnitus (Goebel 1997): expression. Yamamoto et al (1985) reported 20 patients with temporary tinnitus secondary to ● In the brain, tinnitus can be considered as a either facial nerve paralysis or spasm. Facial new signal without a memory. For the brain paralysis and facial neuropathy change the it has, therefore, no cognitive meaning or stapedius muscle activity (intermittent or complementary value (Robson 2002). This is sustained spasms: Bischoff et al 1989, De Souza understood as part of a cognitive/affective et al 1994). Marchiando et al (1983) described clinical picture. Coping strategies such as cases of tinnitus due to stapedial muscle con- fear of irreversible damage to the ear, belief tractions in patients with no concomitant facial in a brain tumour or mental illness are nerve disorders. Cases of tinnitus during not uncommon (Jastreboff 1990). In short, hemifacial spasm are often reported and are tinnitus can be perceived as life threatening possibly due to anomalies of blood vessels in and cause both hyperacusis and phonopho- the posterior fossa or the facial nerve root close bia. Hyperacusis means that daily sounds to the brain (Janetta 1980b, Badia et al 1994). (traffic, kitchen, children, etc.) are exces- sively amplified. This is often accompanied The second part of the literature is predomi- by phonophobia, in which the patient has an nantly about processing mechanisms, particu- excessive fear of daily environmental noise, and worries that these might damage hearing and cause further problems such as head- ache, fatigue and vertigo (Hazell 2001).

Assessment and treatment of cranial nervous tissue 475 ● The worst effect of tinnitus is usually the ● A simple explanation about (central) mecha- distress which increases with time, rather nisms and the natural course of tinnitus. than the tinnitus itself (Goebel 1997). The intensity of unpleasant sensation is depend- ● Positive reinforcement of small personal ent on the strength of emotional influences limitations that are directly related to (limbic system) and the body’s autonomic tinnitus. reaction (Jastreboff 1990). These effects could be headache, fatigue or dizziness. The ● Integration of pain management techniques intensity and quality of the sound is irrele- such as ‘distraction’ or ‘pacing’. vant (Hazell 2002). Figure 17.26 shows this model, based predominantly on central ● Discussion and formulation of subsequent mechanisms (Jastreboff 1990, Jastreboff & goals, together with a programme of con- Hazel 2004). trolling activity, all of which are related to the tinnitus. From this model we learn that a cognitive behaviour strategy such as retraining or expla- Two types of tinnitus are recognized due to nation of benign causes of tinnitus can have a the modulation of nerves in the brainstem, positive influence on the attitude to tinnitus in namely craniocervical and otogenic tinnitus every patient. A specialized programme that (Levine 1999). has proved these effects is the tinnitus retrain- ing therapy (TRT) based on the Jastreboff CRANIOCERVICAL TINNITUS model (Robson 2002). Sensory input comes from: This means that the therapist can integrate craniofacial and cranioneural manual tech- ● The craniofacial region via the trigeminal niques with cognitive behaviour principles nerve (V) and the spinal trigeminal tract such as: (STT). ● The outer and middle ear via the facial (VII), glossopharyngeal (IX) and vagus (X) nerves. Craniocervical tinnitus Otogenic tinnitus V STT Pons VCN DCN Pons DCN VIII VCN VII IX X CST (VII, IX, X) Medulla Medulla C2 MSN MSN FC Spinal cord Spinal cord ab Fig. 17.25 Neurophysiological model of craniocervical and otogenic tinnitus (reproduced with permission from Levine 1999).

476 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT Table 17.4 Management suggestions for disinhibition of the dorsal cochlear nucleus (DCN) Restoration of DCN inhibition Reduction of DCN input Electrical stimulation of the vestibulocochlear nerve (VIII) Transect the output tract of DCN Electrical or mechanical stimulation of somatic pathways Lesion of the DCN Perception and evaluation tribute to the restoration of the inhibition of Auditory and other cortical areas the DCN. ● The effect of input for the vestibulocochlear Detection Emotional associations nerve (VIII) through equilibrium and Subcortical Limbic system balance exercises should be assessed in each individual patient. Source Body Cochlea/brainstem Autonomic nervous system TINNITUS AND VERTIGO Fig. 17.26 Cognitive/affective model showing the In case studies and surveys, vertigo, dizziness possible consequences of tinnitus (reproduced with and tinnitus are often associated with benign permission from Jastreboff 1990). pathology such as acute vestibular dysfunc- tions (Vibert & Häusler 2003), Ménière’s disease ● The craniocervical region via the dorsal (Franz et al 1999), craniocervical dysfunction root. and trauma (Hulse 1994, Nagy & Pontracz 1997, Franz et al 1999, Kessinger & Boneva 2000, ● Fascicular nuclei of the somatosensory Alcantara et al 2002) or craniomandibular dys- medulla (MSN). These converge to a function (Williamson 1990, Chole & Parker common region in the lower medulla, the 1992, Rubenstein 1993, Parker & Chole 1995, medullary somatosensory nuclei (MSN; Lam et al 2001, Alcantara et al 2002). Fig. 17.25). From here fibres project to the DCN and inhibition in the cortex arises. Acoustic neuroma (vestibular schwannoma) which dominantly affects the vestibulococh- OTOGENIC TINNITUS lear nerve can also cause tinnitus together with vertigo. In this case there is a complex of The pathway of otic tinnitus is less compli- symptoms including deep diffuse headache, cated. A loss of input (spontaneous activity) facial nerve paresis, progressive hearing loss from the auditory nerve (VIII) leads to impaired and/or sensitivity changes in the face (Baguley inhibition of the DCN. et al 1997, Matsuka et al 2000, Neff et al 2003). Due to this complication, it is advisable that Treatment suggestions from the dorsal coch- the therapist refer the patient to a neurologist lear nucleus disinhibition hypothesis are men- or ENT specialist as soon as it is clear that the tioned in Table 17.4. patient’s tinnitus and vertigo are not respond- ing to treatment. For the therapist this means that: THE ROLE OF BALANCE EXERCISES FOR ● Manual therapy of the craniofacial and TINNITUS AND VERTIGO craniocervical regions can change the dis- inhibition of the DCN, thus reducing Clinical experience has shown that balance tinnitus. exercises for perception and control of tinnitus can lead to clear improvements. However, ● Treatment by cranioneurodynamics of the there is a lack of effective studies in the litera- trigeminal (V), facial (VII), glossopharyn- ture, hence the following hypotheses: geal (IX) and the vagus (X) nerves can con-

Assessment and treatment of cranial nervous tissue 477 ● Auditory and vestibular afferents have experience with manual craniofacial and neuro- the same projection on the somatosensory dynamic treatment shows that if one technique cortex (Ramachandran & Blakesee 1998). changes and/or reduces the frequency of the Overstimulation of vestibular branches tinnitus, the prognosis is better. filters and muffles the auditory cortex which changes the perception of tinnitus (Hazell ● Equilibrium has to be examined and, if 2002). necessary, integrated into treatment and management. Some research shows that re- ● As an overwhelmed somatic input inhibits education and training of the patient’s equi- the dorsal cochlear nucleus (DCN), the audi- librium makes the tinnitus more acceptable tory cortex receives less stimulation and the and enables the patient to control the tinnitus experienced will be reduced (Levine problem better. Furthermore, balance exer- 1999, Abel & Levine 2004). cises can be used as a kind of ‘distraction’ for the unpleasant sensations in the ear. ● Input from the head, face and neck region, such as balance exercises that do not provoke ● In some cases it is useful to integrate cogni- symptoms, changes the stimuli of the tive strategies alongside manual craniofacial somatosensory cortex (distraction) and in- and cranioneurodynamic techniques. This fluences the activity of the auditory cortex is particularly the case when the manual (Ramachandran & Blakesee 1998). therapy approach changes the tinnitus. The therapist can then provide the patient with ● Systematic information regarding patho- positive feedback and an explanation as genesis and natural course controls tinnitus described under the cognitive/affective and vertigo: most patients experience less model. tinnitus and vertigo during balance exer- cises. This phenomenon can be explained by The therapist must take account of a strong an alertness that may have a positive influ- irritable and latency character of tinnitus in ence on the patient's coping strategies, which some patients. Examination and treatment has in turn can lead to reduced fear and distress to be symptom-free initially. Depending on the (Chatelier et al 1982, Jastreboff 1990, Goebel reaction of the individual patient, the intensity 1997). may be increased. In most cases increasing the duration is more effective than increasing The outcome of standardized balance tests nerve loading. Experiments with facial nerve before and after craniofacial techniques shows techniques combined with occipital and petro- whether tinnitus and vertigo are related in the sal bone pressure medially provide the thera- individual. More information about balance pist with an opportunity to give input into the training can be found in the section about the craniofacial region for a considerable period oculomotor nerves and oculomotor rehabilita- without provoking symptoms. If these tech- tion below. niques change the frequency of tinnitus together with other symptoms, adaptations of MANAGEMENT GUIDELINES FOR them can be used as home programmes and SUBJECTIVE TINNITUS controlled regularly. Besides management by operation, medica- VESTIBULOCOCHLEAR NERVE (VIII) tion, orthodontic dental treatment, psychologi- cal intervention, injection, biofeedback, change Relevant functional anatomy of lifestyle, relaxation therapy, etc., examina- tion and treatment of neurodynamics of the The vestibulocochlear nerve (Fig. 17.27) carries facial nerve, together with passive movements two kinds of specialized sensations: vestibular of neighbouring structures such as palate, sensation (sense of equilibrium including sphenoid, petrosal, temporal and occipital posture and muscle tone) and auditory sensa- bones and/or the craniomandibular region, are suggested (Chan & Reade 1994). Clinical

478 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT N. vestibularis Ganglion vestibulare N. cochlearis Sacculus* Entry of the os temporale Ampullae of the pars petrosa in the semicircular intracranial cavity through canals the pons acusticus internus Semi- circular canals Utriculus* Cochlea * = Sensory cells for linear acceleration Fig. 17.27 Vestibulocochlear nerve. tion from specialized sensory receptors in the STARTING POSITION AND METHOD inner ear. The vestibular nerve originates from the vestibular apparatus and runs for most of The patient lies supine, comfortably and its length together with the auditory nerve relaxed. The therapist sits or stands on the which starts in the cochlea. Together they run right side of the patient’s head. The left hand laterally and are united in the petrosal foramen. cups around the occipital bone which fixes From here they run together with the facial upper flexion and lateroflexion. The right hand nerve from the inner side of the border of the is free for influencing the petrosal and sphe- temporal bone through the internal auditory noid regions. To change the temporal bone meatus and the subarachnoid space. Together region, the starting position as described in the with the glossopharyngeal nerve they enter method needs to be changed. the lateral dorsal side of the brainstem (Silver- stein & Jackson 2002). For examination of the petrosal bone, bend over the patient and, with the thumb and the Neurodynamic test flexed index finger, grasp around the contra- lateral bone. Every accessory movement The neurodynamic test of the vestibulococh- required can now be performed. Make sure lear nerve is not really spectacular because the that the head position does not change. nerve runs 100% intracranially. If the history and the symptoms fit in with a possible dys- For movement of the occipitosphenoid region function of the vestibulocochlear nerve, the in this position, the therapist faces the patient. proposed neurodynamic test together with The left hand is in supination and cups the neural container assessment can be performed. occipital bone. The right thumb and index finger To load the nerve, upper cervical flexion and grasp around the lateral side of the sphenoid lateroflexion are necessary. Accessory move- bone (Fig. 17.28). In this position the main acces- ments of the petrosal, occiput, sphenoid and sory movements of the occipitosphenoid region temporal bones can all influence the vestibulo- can be performed. The best position for access to cochlear nerve which is intracranially con- the temporal bone is sitting above the patient’s nected with the lateral side of the cranium head. The left hand holds the required head (temporal region). position to load the cranial nervous tissue on the left side. With the right hand, grasp the temporal bone with the right middle finger in the ear

Assessment and treatment of cranial nervous tissue 479 Fig. 17.28 (Part of the) neurodynamic test of the a vestibulocochlear nerve. Sphenoid examination in craniocervical neurodynamic position. canal, the right little finger on the petrosal bone b and the auricular extension, and the right thumb on the region above the ear. All movements Fig. 17.29 Examination of auditory function using a described in Chapter 15 may influence the symp- tuning fork. toms which may come from pathophysiological a Rinne test. changes of the vestibulocochlear nerve. b Weber test. Palpation The Rinne test The vestibulocochlear nerve runs 100% intra- The therapist strikes a tuning fork, holds it near cranially and is not palpable. one external meatus, covering (± 2–3 cm) the other, and asks the patient if they can hear it. Conduction The therapist then alternates the position of The purpose of the conduction test is to reveal the tuning fork from the mastoid process to in either a middle-ear hearing problem or reduced front of the ear, until the note is no longer nerve activity. Balance impairments, if these audible in any position (Fig. 17.29a). With originate from the labyrinth, vestibular nerve normal conductivity, the tone can be heard or the brainstem, are more dispersed and often longer in front of the ear than on the mastoid have a predictable pattern. In this case the process (negative Rinne test). When the tuning patient should be referred to an ENT fork can be heard for longer on the mastoid specialist. process than in front of the ear this is abnormal (positive Rinne test). This reaction THE FUNCTION OF THE AUDITORY NERVE Examination of hearing The therapist gently rubs the tips of the index finger and thumb together 2–8 cm from the patient’s ears and asks the patient if the sound produced is heard equally in each ear. If there is a loss or diminished response on one side, differentiation of the localization of the deaf- ness can be achieved by a tuning fork using Rinne’s and Weber’s tests.

480 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT indicates a hearing defect in the middle ear or neural hearing loss (related to the acoustic nerve). In this case the Weber test must be carried out. The Weber test The tuning fork is placed on the centre of the frontal bone (Fig. 17.29b). The patient is asked if they can hear the sound all over the head, in both ears or mainly in one ear. In nerve ‘deaf- ness’ the sound appears to be heard in the normal ear but in chronic middle ear disease the sound is conducted to the normal ear. ● When changes of neurodynamic position alter the hearing during the Weber test, neurogenic dysfunction rather than middle ear disease is indicated. ● Hearing disturbance caused by the audi- tory nerve (VIII) together with conduction symptoms of the trigeminal (V) and facial (VII) nerves are probably due to lesions or pathodynamics of the cerebellopontine angle (Spillane 1996). ● Bilateral deafness during the Weber test may be due to bilateral middle ear disease or a central lesion (Spillane 1996). On discovery of any of these clinical patterns, further assessment by a neurologist or otolaryn- gologist is imperative (Berghaus et al 1996, Halmagyi 2005). If no clear pathology is found, manual assessment of the craniofacial region can be an option (Berghaus et al 1996). FUNCTION OF THE VESTIBULAR NERVE: Fig. 17.30 Progression of the two leg standing test; EQUILIBRIUM TESTS WITH OR WITHOUT here with one foot in front and one behind with the NEURODYNAMIC POSITION eyes closed. Two legs standing test Let the patient stand on two legs with a rela- tively small support base, i.e. feet together or one foot in front of the other (Fig. 17.30). In this position neurodynamic loading of the head is added. In the author’s opinion upper cervical flexion is the best position. Passive neck flexion must always be assessed separately. If symptoms such as vertigo, balance prob- lems, falling, nystagmus and ‘seeing stars’ occur, the hypothesis is a conductive impair-

Assessment and treatment of cranial nervous tissue 481 ment of the vestibular (VIII) nerve. Latero- flexion to the other side can be helpful; however, this also influences the semicircular canals of the balance organ (Spillane 1996). Other standardized balance tests such as the Romberg, Unterberger, rope dancer and Stern tests can be used. The head position can be varied, for example in upper cervical flexion or lateroflexion to the opposite side. ! The therapist should be aware that the neurodynamics of the vestibular (VIII) nerve is not the only aspect affected. The capsule and endolymph in the semicircular canals of the labyrinth are also affected. These stimulate input of the cochlear compo- Fig. 17.31 Observation of nystagmus with Frenzel nents and the vestibulocochlear nerve (Wilson- glasses after the rotation test. Pauwels et al 2002). If abnormal reactions such as stiffness or pain occur during the neuro- The temperature test dynamic investigation, treatment without increase of vertigo or light-headedness is an This test is a general test for the vestibulo- option. ocular reflexes. Warm saline is placed in the ear. If it results in nystagmus, referral to a neu- Re-examination of symptom behaviour and rologist is indicated. standardized balance tests can confirm or dis- prove the relevance of abnormal neurodynamic Comment reactions. More information on balance tests and oculomotor rehabilitation is given in the The vestibular nerve has a relatively long section on the oculomotor system. intracranial course and multifarious internal interactions with the vestibular muscles within The rotation test the nervous system. Therefore there are numer- ous potential causes for light-headedness, This is a test for the vestibular apparatus on vertigo, ear pain after middle ear inflamma- both sides. The patient is seated in a swivel tion and balance impairment. These could be chair which is rotated ten times in 20 seconds. impaired vascularization, metabolism, degen- The patient’s head is well supported and held erative compression and neoplastic lesions in 30% flexion. Nystagmus, ‘seeing stars’ and of the vestibulocochlear brainstem complex falling to the ipsilateral side or an increase of (Torok & Kumar 1978, Mafee et al 1984, tinnitus can be an indication of overstimula- Schwaber & Whetsell 1992). tion of the labyrinth (Baloh et al 1984, Saadat et al 1995, Spillane 1996). As most nystagmus usually cannot be observed with the naked eye (Berghaus et al 1996), the therapist needs a pair of Frenzel glasses. This is an instrument with magnifying glasses and a small light on the inside. This magnifies the eyes so that eye movements can be seen more easily (Fig. 17.31).

482 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT VASCULARIZATION man, the presence of perivascular inflamma- tion (vasculitis) could be responsible for this Recent magnetic resonance (MR) imaging HIV-1 associated cranial nerve neuropathy. reports show that inflammation in the areas Uneven disturbances of local ischaemia may of the anterior inferior cerebellar artery explain the scattered occurrence of axon degen- (AICA) and the posterior inferior cerebellar eration and segmental demyelination which artery (PICA) reproduce signs and symptoms contribute to destruction of the nerves (Nukada similar to vestibulocochlear nerve neuropathy & Dick 1984). If a patient complains of sudden (Nakayama et al 1989, Kido et al 1994, Laine & bilateral hearing loss, dizziness and/or a deep Underhill 2002). This is because these arteries cranial pain of sudden onset, it may be wise to supply the cerebellum, the lower part of the ask a neurologist or ENT specialist for a dif- pons, the upper part of the medulla oblongata ferential diagnosis. Whether the neurodynam- and the inner ear (Atkinson 1949, Naidich et al ics of cranial nervous tissue can change due to 1976). These arteries lie parallel to the flexion– pathophysiology and mechanical scar tissue extension axes and are influenced by upper or adhesions which occur following a severe cervical flexion and side flexion (Breig 1976, inflammation around blood vessels is still not Jannetta 1990). This knowledge can be linked clear. to the question of why, during and after upper cervical flexion and side flexion, symptoms TUMOURS such as dizziness, tinnitus and ear pain change, especially when a cranium technique of the Acoustic neuromas, which account for 80–90% sphenoid and/or occipital bone is added. Vas- of cerebellopontine angle (CPA) tumours cular occlusion disturbances due to compres- (Rowland 1989), are the most common of the sion because of anomalies and degeneration posterior fossa tumours (Langman et al 1990). are possibly eliminated or lessened for a while The tumour usually begins on the vestibulo- during these gentle unloading techniques of cochlear nerve in the CPA and the trigeminal the dorsal side of the cranium. This could be and facial nerves are affected more often than an alternative hypothesis as to why this hap- other cranial nerves (Langman et al 1990, pened (Breig 1960, 1976, Gorge 2001). Normand & Daube 1994, Sanna et al 2003). A patient who presents with symptoms such as METABOLIC CHANGES facial numbness, facial palsy, decreased corneal reflex and facial pain (Eisen & Danon 1974, Viral infections can cause sudden dysfunction Ylikoski et al 1981, Nager 1985, Fischer et al of cranial nerves. Ocular (Fuller et al 1989) and 1992), which increase with head correction into facial (Wechsler & Ho 1989) nerve involvement upper cervical flexion and contralateral latero- are clearly reported with increasing evidence. flexion, is not indicated for treatment by Temporal bone studies of patients during neurodynamics. and after vestibular neuritis have highlighted maximal damage in the dural branches of the Needle electromyography of cranial nerves vestibular nerve where the changes are felt to is used to diagnose the acoustic neuroma be consistent with a viral aetiology. Several (Nager 1985, Harner et al 1987, Armon & Daube viruses (e.g. rubella, herpes simplex, reovirus, 1989, Normand & Daube 1994) and surgical neurotrophic influenza and mumps) can infect removal (Fischer et al 1980, Cohen et al 1986, the vestibular nerve and its environment Glasscock et al 1986, Burchiel et al 1988, (Davis 1993). In the past two decades, the Shelton et al 1989) or stereotactic radiosurgery human immunodeficiency virus (HIV) has (Bederson et al 1991, Flickinger et al 1992, been very evident, but the pathogenesis is cur- Linskey & Sekhar 1993, Ogunrinde et al 1994) rently unknown (Simpson & Bender 1988, will be the treatment of choice (Fischer et al Chaunu et al 1989, Grimaldi et al 1993). 1980, Cohen et al 1986, Glasscock et al 1986, Grimaldi et al (1993) showed that, in a biopsy Burchiel et al 1988, Shelton et al 1989). On the of the dural nerve of an HIV-1 seropositive other hand, an iatrogenic factor of surgery in

Assessment and treatment of cranial nervous tissue 483 the CPA may be vestibular and facial neuropa- tebral artery whereas extension alone did not thies (Flickinger et al 1992, Linksey & Sekhar (Toole & Tucker 1960, Brown & Tatlow 1963). 1993). In dogs it is proven that the caudal to Krueger and Okazaki (1980) conclude that the posterior shift of the nerve trunk may avulse occlusion of the vertebral artery was unpre- the vestibular nerve. Cranial neurodynamics dictable during flexion and rotation of the performed passively or actively may be a good cervical spine. Lateroflexion produces a small complementary therapy after cerebellopontine occlusion change and flexion, together with angle surgery. lateroflexion, has minimal influence on nar- rowing (Gutmann 1983b, Bolton et al 1990). DIZZINESS AND VERTIGO There are still patients who are dizzy in Dizziness and vertigo are some of the most flexion and other positions combined with common symptoms for which a patient will lateroflexion and any small amount of rotation, consult a primary care therapist (Douglas without a clear history of overstimulation of 1993). Dizziness can be described in general the proprioceptive system of the upper cervical terms, implying only the sense of a disturbed spine (Terrett 1983). For example, symptoms relationship to the space outside oneself (Smith during computer work, reading in bed with the 1990); vertigo can be described as the illusion hand on the lateral side of the face, putting on of motion or position, either of the patient or shoes, etc. whereby the patients feels that the the patient’s environment (Adams & Victor head position and the movement influencing 1985, Fowler & May 1985). They are often the dizziness may be cervicogenic in origin; accompanied by other associated symptoms however, another possibility could be patho- such as tinnitus, nausea, vomiting, nystagmus, physiological changes of the vestibular nerve. perspiration, a sense of fear, diplopia, drop attacks, dysarthria, dysphagia, tiredness, etc. Vestibular neuritis is the second most (Coman 1986, Oostendorp 1988, Hanson 1989, common cause of vertigo. The superior divi- Douglas 1993, Roy 1994). Further detailed sion is mainly affected, including the afferent information about anatomy, pathophysiology, from the horizontal and anterior semicircular common differential diagnostic considerations canals (SCC) (Fetter & Dichgans 1996). Upper and aetiology is reviewed in good fundamen- cervical flexion and lateroflexion of the cervi- tal literature in this domain and will not be cal spine change the pressure in the CPA and discussed further here (Troost 1980, Gutmann the vestibular nerve (Breig 1960, 1976, Jannetta 1983a, Oostendorp 1988, Patten 1995, Grant et al 1984, Leblanc 1995). In some cases, where 1996). the patient provokes vertigo or dizziness in a flexed head position (or keeps the head in For the therapist it can be interesting to note slight neck extension to prevent these symp- which head positions influence the dizziness toms), it could be useful to examine the in order to gain information about which neurodynamics of the cranial nerve tissue, structures are involved. For example, there are especially that of the vestibulocochlear nerve. good clinical protocols for vertebral artery As treatment using neurodynamics often pro- testing whereby the therapist gets an indica- vokes reactions of severe dizziness or vertigo, tion of the condition of the vertebrobasilar the therapist must bear these facts in mind and complex before manual therapy on the cervical is recommended to start without resistance in spine is carried out (Maigne 1972, Gutmann the direction of the neurodynamic position or 1983a, Maitland 1986, Aspinall 1989, Douglas to treat the cranial bones out of a loaded posi- 1993, Grant 1996). tion (upper extension, ipsilateral lateroflexion of the head) without symptoms. Gutmann (1983b) argued that flexion and extension of the cervical spine have no influ- Generally, if the symptoms change, either ence on the narrowing of the vertebral artery. during or after this test, this is a good indica- On the other hand, extension combined with tion for further examination and treatment. In cervical rotation produced occlusion of the ver- the case of severe and irritable symptoms such

484 CRANIOFACIAL PAIN: NEUROMUSCULOSKELETAL ASSESSMENT, TREATMENT AND MANAGEMENT as nausea and vomiting, tinnitus, vertigo, etc. bution of the vagus nerve. Inside the skull, it is best first to treat the petrosal or temporal both these components join forces and exit bone in an unloaded position for the vestibulo- through the jugular foramen. Once outside the cochlear nerve. Studies show that mechanical skull they pass the styloid process medially. impulses on the cranial bones activate the ver- Some branches terminate in the sternocleido- tebral apparatus (Ito et al 1990, Halmagyi et al mastoid muscle. The nerve then crosses super- 1995, Manni et al 1996). On the other hand, in ficially to the posterior triangle of the neck, to the author’s opinion, otovestibular symptoms the levator scapulae. This is the optimal point such as otalgia, sensitivity to loud noise or for palpation. Many anomalies are seen; for muffled hearing without underlying pathol- example, some branches meet above and run ogy such as infection, tumours, etc., react better deep to the anterior edge of the trapezius to to indirect techniques with little resistance supply this muscle (Fig. 17.33). Many anoma- (e.g. hard palate mobilization in or out of load position of the eighth cranial nerve). Table 17.5 Overview of the physical examination options for the vestibulocochlear Table 17.5 gives a general overview of the nerve (VIII) physical examination options for the vestibulo- cochlear nerve. Neurodynamic tests Conduction tests ACCESSORY NERVE (XI) Craniocervical: Auditory nerve: Upper cervical flexion Examination of hearing Relevant functional anatomy Contralateral lateral Rinne’s, Weber’s test flexion The accessory nerve is a motor nerve consist- ing of a spinal and a cranial component (Fig. Craniofacial: Vestibular nerve: 17.32). The spinal component is derived from a Petrosal Two leg standing test number of upper cervical spinal nerve roots Temporal Other balance tests which arise from the five uppermost cervical Sphenoid Rotation test segments and pass through the foramen Occiput Temperature test magnum to access the skull. The cranial com- ponent is integrated into the peripheral distri- Cranial radix Vagus nerve Jugular foramen Foramen magnum Sternocleidomastoid muscle Spinal radix Trapezius muscle Fig. 17.32 Accessory nerve.