Skull, Face and Neck

Part 5 · Head, neck and the nervous system

The skull, the TMJ, the muscles of facial expression, and the triangles of the neck

What this region gives a physiotherapist

Three caseloads live in this chapter.

Facial palsy. Bell’s palsy has an annual incidence of around 20–30 per 100,000 and most cases recover — but the ones that do not need facial retraining, and the difference between an upper and a lower motor neuron lesion is decided by a single anatomical fact about the forehead.

Temporomandibular disorders. They affect around 5–12% of the population, are the second commonest musculoskeletal pain condition after low back pain, and respond well to conservative management — yet most physiotherapists feel unqualified to treat them because the anatomy was taught as dentistry.

The neck. Cervicogenic headache, cervicogenic dizziness, whiplash, thoracic outlet syndrome, torticollis and post-neck-dissection shoulder dysfunction all require the anatomy of the triangles, the fascial planes and the cranial nerves that traverse them. So does the cervical arterial screening every clinician must perform before treating a neck.

Learning outcomes

• Describe the bones of the skull, the sutures, fontanelles and cranial fossae.
• Describe the principal foramina of the skull base and their contents.
• Describe the temporomandibular joint and its two-compartment mechanics.
• Describe the muscles of mastication and facial expression, with nerve supply.
• Distinguish upper from lower motor neuron facial palsy and explain the anatomical basis.
• Describe the triangles of the neck and their contents.
• Describe the cervical fascia and its clinical significance.
• Describe the vertebral and carotid arteries and their clinical assessment.
• Explain temporomandibular disorders, cervicogenic headache and dizziness, torticollis and thoracic outlet syndrome.

The skull

Figure 1 · The skull

22 bones (excluding the auditory ossicles), in two functional groups.

Developmental origin: the vault and most facial bones ossify in membrane (from neural crest ectomesenchyme for the face); the skull base ossifies in cartilage (chondrocranium). This is why the vault can mould during birth and why base growth follows synchondroses.

Sutures and fontanelles

Fontanelle

Position

Closes

Anterior (bregma)

Coronal + sagittal, diamond-shaped, the largest

~18 months

Posterior (lambda)

Sagittal + lambdoid, triangular

~2–3 months

Sphenoidal and mastoid

Lateral

~6 months and ~1–2 years

Clinically: the anterior fontanelle is a window for ultrasound and a bedside indicator — bulging in raised intracranial pressure, sunken in dehydration. Premature sutural fusion is craniosynostosis, producing a characteristic skull shape depending on which suture fuses.

The pterion — the H-shaped junction of the frontal, parietal, temporal and greater wing of sphenoid, on the temple about 4 cm above the zygomatic arch — is the thinnest part of the skull and overlies the anterior division of the middle meningeal artery. A blow here causes an extradural haematoma, classically with a lucid interval followed by rapid deterioration. It is the single most examined point of skull surface anatomy.

The cranial fossae and their major foramina

Mnemonic for the foramen ovale contents: OVALE — Otic ganglion above, V3, Accessory meningeal artery, Lesser petrosal nerve, Emissary veins.

The mandible is the only mobile skull bone. Its condylar process articulates at the TMJ; its coronoid process takes temporalis; the angle takes masseter laterally and medial pterygoid medially; the mandibular foramen on the medial ramus transmits the inferior alveolar nerve (the dental block site), which emerges at the mental foramen. The mental, infraorbital and supraorbital foramina lie roughly in a vertical line — the three exit points of the trigeminal cutaneous branches, and the standard palpation points for trigeminal sensory testing.

The temporomandibular joint

A synovial joint with unique features: it is bilateral and must move as a pair, its articular surfaces are covered by fibrocartilage rather than hyaline cartilage (because the bones develop in membrane), and it is divided into two functional compartments by a disc.

Two compartments, two movements

Lower compartment: rotation. Upper compartment: translation.

• The first ~20–25 mm of mouth opening is rotation in the lower compartment.
• Beyond that, the condyle and disc translate together anteriorly down the articular eminence in the upper compartment, to complete opening.

Normal opening is 40–50 mm (approximately three of the patient’s own fingers vertically); lateral excursion and protrusion are ~10 mm each. Opening under 35 mm is restricted.

Movements: depression, elevation, protrusion, retrusion, and lateral excursion. Lateral excursion is asymmetrical — the ipsilateral condyle rotates while the contralateral condyle translates forward and medially, which is why unilateral pathology produces deviation.

The muscles of mastication

All four are supplied by the mandibular division of the trigeminal nerve (V₃).

Also assisting depression: the suprahyoid muscles (digastric, mylohyoid, geniohyoid, stylohyoid) when the hyoid is fixed by the infrahyoids — which is why jaw, hyoid, tongue and cervical posture are mechanically coupled, and why forward head posture alters mandibular resting position.

Temporomandibular disorders

Assessment: measure opening, note deviation (towards the restricted side) or deflection, palpate masseter, temporalis and the lateral pterygoid region, auscultate for click or crepitus, and always examine the cervical spine — the upper cervical spine and the TMJ share trigeminocervical convergence (§22.7) and their symptoms overlap constantly.

Management is conservative first-line and effective: education and reassurance, parafunction awareness, jaw rest within a comfortable range, controlled active exercise and manual therapy, postural and cervical management, and stress and sleep management. Occlusal splints have a role, and irreversible occlusal or surgical intervention should follow, not precede, conservative care.

Muscles of facial expression, and facial palsy

Figure 2 · Why a stroke spares the forehead

All are supplied by the facial nerve (CN VII) and develop from the second pharyngeal arch. They are unusual in inserting into skin rather than bone, which is what allows expression.

The facial nerve

Course: brainstem → internal acoustic meatus → facial canal in the petrous temporal bone (giving the greater petrosal nerve, the nerve to stapedius, and the chorda tympani) → stylomastoid foramen → through the parotid gland, where it divides into five terminal branches.

Terminal branches: Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical — “Ten Zebras Bit My Curls” or “Two Zulus Buggered My Cat” (both are in circulation; use whichever you can say in an exam).

Functions: motor to the muscles of facial expression, stapedius, stylohyoid and the posterior belly of digastric; taste from the anterior two-thirds of the tongue (chorda tympani); parasympathetic secretomotor to the lacrimal, submandibular and sublingual glands; and a small sensory patch at the external acoustic meatus.

The forehead rule — upper versus lower motor neuron facial palsy

The part of the facial nucleus supplying the upper face (frontalis and orbicularis oculi) receives BILATERAL corticobulbar input; the part supplying the lower face receives only CONTRALATERAL input.

Therefore:

This single sign — forehead sparing — distinguishes a stroke from a Bell’s palsy at the bedside, and a physiotherapist must be able to make that distinction. A patient presenting with a facial droop and an intact forehead requires urgent stroke assessment, not facial exercises.

Bell’s palsy — idiopathic (probably viral, HSV-1 reactivation) lower motor neuron facial palsy, of acute onset over hours. Around 70–85% recover fully, most within 3 weeks to 3 months. Corticosteroids started within 72 hours improve outcome (Sullivan et al., NEJM 2007); antivirals add little.

Physiotherapy role:

• Eye protection is the first priority — artificial tears, ointment and taping at night. Corneal ulceration is the serious avoidable complication
• Facial retraining: mirror feedback, slow, small-amplitude, specific movements; avoid gross, forceful, maximal-effort exercise and avoid electrical stimulation, both of which are associated with synkinesis (aberrant reinnervation producing involuntary co-movement — the eye closing when the mouth moves)
• Grading: House–Brackmann (I–VI) or the Sunnybrook Facial Grading System (more responsive, and preferable for tracking change)
• Mime therapy and neuromuscular retraining have the best evidence in persistent and synkinetic cases

The triangles of the neck

Figure 3 · The triangles of the neck

Sternocleidomastoid divides each side into an anterior and a posterior triangle.

Two clinically critical points in the posterior triangle

1. The spinal accessory nerve is extremely superficial. It crosses the posterior triangle in the investing fascia, roughly from the junction of the upper and middle thirds of the posterior border of SCM to a point 5 cm above the clavicle on trapezius. It is the nerve most commonly injured by minor surgery in the neck — a lymph node biopsy in the posterior triangle is a classic cause. The result is trapezius palsy: a drooping shoulder, lateral winging, and inability to elevate the arm fully (Chapter 10). Physiotherapists see these patients, and the history of a small neck operation is the clue.

2. Erb’s point — where the four cutaneous branches of the cervical plexus (lesser occipital, great auricular, transverse cervical, supraclavicular) emerge around the middle of the posterior border of SCM. It is the landmark for a superficial cervical plexus block. (The name is also used for a different point over the upper trunk of the brachial plexus — context matters.)

Key muscles of the neck

The deep cervical flexors deserve emphasis. The craniocervical flexion test (using a pressure biofeedback unit) reliably identifies reduced deep flexor activation and increased superficial (SCM, scalene) substitution in people with neck pain and whiplash. Low-load deep flexor retraining has good trial evidence for reducing neck pain and cervicogenic headache — one of the better-supported specific exercise interventions in musculoskeletal physiotherapy.

Cervical fascia and vessels

Figure 4 · Cross-section of the neck

The fascial layers

The arteries

Common carotid — bifurcates at the upper border of the thyroid cartilage (C4) into:

• External carotid — eight branches (Some Anatomists Like Freaking Out Poor Medical Students: Superior thyroid, Ascending pharyngeal, Lingual, Facial, Occipital, Posterior auricular, Maxillary, Superficial temporal). The maxillary artery gives the middle meningeal artery
• Internal carotid — no branches in the neck; enters the carotid canal, traverses the cavernous sinus, and supplies the brain and orbit

The carotid sinus (at the bifurcation) is a baroreceptor supplied by the glossopharyngeal nerve; the carotid body is a chemoreceptor. Carotid sinus hypersensitivity means firm pressure over the bifurcation can cause bradycardia and syncope — a reason to avoid heavy anterolateral neck pressure in older patients.

Vertebral artery — the first branch of the subclavian, ascending through the foramina transversaria of C6 to C1, then turning sharply medially in the groove on the posterior arch of the atlas before entering the foramen magnum to form the basilar artery. It supplies the brainstem, cerebellum and posterior cerebrum.

Cervical arterial dysfunction — the screening every clinician must do

The vertebral artery is most tortuous and most mechanically stressed in the atlanto-axial segment, where it is stretched by rotation and by rotation with extension. Cervical arterial dissection — vertebral or internal carotid — is rare but catastrophic, and it presents with neck pain and headache before any neurological sign, which is exactly why patients present to physiotherapists.

The IFOMPT framework has replaced pre-manipulative positional testing (which had poor validity) with a reasoning process across the whole examination:

• History: sudden severe unfamiliar neck pain or headache (“unlike any I’ve had”), recent trauma or manipulation, vascular risk factors (hypertension, smoking, hyperlipidaemia, clotting disorder, migraine, recent infection)
• The 5 Ds and 3 Ns: Dizziness, Diplopia, Dysarthria, Dysphagia, Drop attacks; Nausea, Nystagmus, Numbness (especially perioral). Also ataxia and facial palsy
• Examination: blood pressure, cranial nerve screen, and observation of any neurological sign during positional testing — but a negative positional test does not clear the patient

The clinical rule: if the presentation is a new, unusual, severe headache or neck pain — particularly with any of the above features — it is a medical presentation until proved otherwise, and end-range rotation techniques and manipulation are contraindicated.

Clinical conditions

Cervicogenic headache

Mechanism: the trigeminocervical nucleus. The spinal nucleus of the trigeminal nerve extends caudally into the upper cervical cord and converges with the afferents from C1, C2 and C3. Nociceptive input from upper cervical structures — the atlanto-occipital and atlanto-axial joints, the C2–C3 facet joint, the suboccipital muscles, the upper cervical discs and dura — is therefore perceived as head pain in trigeminal territory.

Features: unilateral, side-consistent headache, starting in the neck and radiating fronto-orbitally; provoked by neck movement or sustained posture; reduced cervical range (especially the flexion-rotation test, which specifically assesses C1–C2 and is the single most useful test); tenderness of the upper cervical segments.

Management has good trial evidence (Jull et al.): manual therapy plus low-load craniocervical flexor and scapular retraining, sustained over 6 weeks, with effects maintained at 12 months.

Cervicogenic dizziness

A diagnosis of exclusion, made after vestibular and vascular causes are ruled out. The mechanism is disturbance of cervical proprioceptive input — the deep upper cervical muscles have among the highest muscle spindle densities in the body (Chapter 17), and their afferents converge with vestibular and visual input in the central integrator. Altered or asymmetrical cervical input therefore produces sensory conflict, experienced as unsteadiness or light-headedness.

Distinguishing features: dizziness described as unsteadiness or disorientation rather than true spinning, temporally related to neck pain and neck position, lasting minutes to hours, without hearing loss or true nystagmus. Managed with cervical treatment plus oculomotor and cervical joint position sense retraining, which has supportive evidence.

But rule out first: BPPV (positional, brief, rotatory, with a positive Dix–Hallpike), vestibular neuritis, Ménière’s, orthostatic hypotension, medication, and — critically — vertebrobasilar insufficiency or dissection.

Torticollis

Thoracic outlet syndrome

Compression of the neurovascular bundle at three possible sites:

Types: neurogenic (~95%, but true neurogenic TOS with objective wasting is rare), venous (~3%, Paget–Schroetter effort thrombosis), arterial (~1%, but the most serious). A cervical rib or fibrous band is present in a minority.

Provocation tests (Adson’s, Roos/EAST, Wright’s, costoclavicular) all have poor specificity — they are positive in a substantial proportion of asymptomatic people — so diagnosis rests on the pattern, and on excluding cervical radiculopathy and peripheral entrapment. Management is postural, scalene and pectoralis minor loading and length work, nerve gliding, and breathing pattern retraining.

Cranial nerve overview (detailed in Chapter 23)

Worth noting here which cranial nerves a physiotherapist tests routinely and why: V (facial sensation, masticatory power), VII (facial expression, forehead rule), VIII (hearing and vestibular function), IX/X (swallow, gag, palate), XI (trapezius and SCM), XII (tongue). Together they form the bulbar screen that determines swallow safety and stroke localisation.

Where students consistently go wrong

• Forgetting the pterion overlies the middle meningeal artery.
• Getting the two TMJ compartments backwards. Lower = rotation, upper = translation.
• Forgetting lateral pterygoid is the odd muscle — it opens rather than closes the jaw.
• Not knowing the forehead rule. It distinguishes stroke from Bell’s palsy at the bedside.
• Prescribing forceful facial exercise or electrical stimulation in Bell’s palsy — both are associated with synkinesis.
• Neglecting eye protection in facial palsy. Corneal ulceration is the avoidable disaster.
• Forgetting how superficial the spinal accessory nerve is in the posterior triangle.
• Getting SCM’s action backwards. Ipsilateral lateral flexion with contralateral rotation.
• Relying on pre-manipulative positional testing to “clear” the vertebral artery. Use the whole clinical reasoning framework.
• Treating a new, severe, unfamiliar headache with neck pain as mechanical.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 22 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 23 — The Nervous System: brain, spinal cord, tracts and the cranial nerves.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents