Anatomy

It is useful to consider the anatomy of the nose by dividing it into:

External nose

The upper third of the external nose (Fig. 2.1) is bony, consisting of nasal bones which connect with the nasion at the forehead. The inferior two-thirds are cartilaginous, consisting of the upper lateral and lower lateral (alar) cartilages. The tip laterally contains resilient but pliable fibrocartilage. This allows maintenance of nasal shape after minor trauma. The skin over the cartilaginous portion is closely adherent and contains multiple sebaceous glands; these latter structures may hypertrophy to form a rhinophyma.

Fig. 2.1 Constituent elements of the external nose.

Nasal cavity

The nasal cavity stretches from the vestibule anteriorly to the nasopharynx posteriorly and is divided by a midline osteocartilaginous septum. The lateral wall of the cavity supports a series of ridges called turbinates (Fig. 2.2). These structures are lined by ciliated columnar epithelium and contain erectile tissue. The paranasal sinuses – maxillary, frontal, ethmoid and sphenoid – drain into the nasal cavity around the middle turbinate.

Fig. 2.2 Structure of the lateral wall of the nasal cavity.

The nasal septum comprises bony and cartilaginous elements. Inferiorly, it is inserted into a groove in the maxillary crest (Fig. 2.3). It is lined with mucoperichondrium and mucoperiosteum over the cartilage and bone, respectively. The nasal septum is rarely straight; marked displacement causes nasal airway blockage and an external cosmetic deformity.

Fig. 2.3 The nasal septum.

Vascular and nerve supply

Both the external and internal carotid arteries supply the nose via their terminal branches. As a guideline, the region above the root of the middle turbinate is supplied by the anterior and posterior ethmoidal arteries, with the remaining areas being supplied by the sphenopalatine, palatine and labial arteries. The carotid system anastomoses at the anteroinferior region of the septum are called Little’s area or Kiesselbach’s plexus.

Venous drainage of the external nose is of importance, as blood can drain via the facial and ophthalmic veins to the cavernous sinus. Therefore, a superficial infection of the nasal lining may involve the cavernous sinus.

The main sensory supply is via the maxillary division of the trigeminal nerve. Secretory glands are under the control of the autonomic nervous system in the vidian nerve. The nasal vascular supply is constricted by sympathetic nerve stimulation and dilated by parasympathetic.

Physiology

Anatomy

The paranasal sinuses (Fig. 2.4) are really extensions of the nasal cavity as air-filled spaces into the skull bones. Although paired anatomically, from a pathophysiological view they should be grouped as anterior and posterior. The frontal, anterior ethmoidal and maxillary sinuses (anterior group) drain into the middle meatus, and the posterior ethmoidal and sphenoid (posterior group) drain into the superior meatus and sphenoethmoidal recess. The crucial drainage area of the anterior group of paranasal sinuses is called the ostiomeatal complex (Fig. 2.4). The nasolacrimal duct opens into the anterior part of the inferior meatus.

Fig. 2.4 The paranasal sinuses.

Physiology

No specific function has been attributed to the paranasal sinuses. The following have been considered:

Nasal obstruction

Nasal obstruction is the most common symptom, and may be due to anatomical abnormalities, disorders of the mucous membrane lining or stimulation of the autonomic nervous system (Table 2.1). An allergic aetiology is likely where the symptoms manifest after contact with allergens such as grass pollen, feathers or animal dander. Viral infections, e.g. acute coryza and influenza, cause severe nasal obstruction but generally resolve rapidly over days. An overactivity of the parasympathetic as compared to the sympathetic nerve supply will cause dilatation of the vascular tree and hence engorgement. This is particularly noted by some patients in stress situations and with alterations in ambient temperature and humidity. Neoplasia produces a progressive unilateral obstruction.

Table 2.1 Causes of nasal obstruction

Nasal discharge

The specific character of the discharge is helpful in deciding aetiology (Table 2.2). Many patients describe this as ‘catarrh’. However, if it produces a runny nose, the discharge should be described as rhinorrhoea and the term ‘catarrh’ (or postnasal drip) reserved for nasal discharge passing backwards into the nasopharynx. Epistaxis is nasal haemorrhage and is most commonly due to spontaneous rupture of a blood vessel in the nasal mucous membrane. However, it is vital to exclude any bleeding disorders and neoplasms. If the discharge is offensive, it may indicate a bacterial infection, the presence of a foreign body or neoplasia.

Table 2.2 Nasal discharge: its characteristics and significance

Sneezing

Sneezing is a frequent accompaniment of allergic and infective rhinitis. Patients with allergies to household dust and dust mite sneeze on awakening, as the bed mattress forms a huge reservoir of allergens.

Facial pressure/pain

It is uncommon to see facial pain due to a local cause such as nasal vestibulitis or herpes eruption. More frequently it is related to disease in the distribution of the trigeminal nerve, which supplies the sensory component to the face and the interior of the nose and paranasal sinus via the ophthalmic and maxillary nerves.

Otological

Any pathological process that disrupts the function of the Eustachian tube may give rise to aural symptoms. Nasal polyps, particularly of the antrochoanal variety, can physically block the pharyngeal end of the tube. Allergic diseases result in a similar problem by provoking oedema, and neoplasms may directly invade the Eustachian tube. The most frequent otological symptom is hearing loss caused by a middle ear effusion secondary to Eustachian tube dysfunction.

Disorders of smell

Anosmia, a total loss of sense of smell, is rare. Hyposmia, a reduced sense of smell, is more common.

Cacosmia, which is an unpleasant smell detected mainly by others, may be caused by chronic nasal sepsis. Ozaena, a foul smell, is a common complaint in anaerobic infections seen in cases of atrophic rhinitis, but the presence of a foreign body and tumour must be excluded.

Halitosis

Poor dental hygiene and diet are the most common causes of halitosis. However, chronic sinusitis with purulent postnasal drip can produce this symptom (p. 51).

External

Certain cosmetic deformities such as angulation of the bony nasal pyramid or a nasal hump may be obvious. A saddle deformity due to previous injury or infection is readily identified. It is not unusual to find the septal cartilage dislocated into the nasal vestibule (Fig. 2.6).

Fig. 2.6 Functional and cosmetic deformities of the nose. (a) The caudal end of the nasal septum is dislocated into the right nostril. (b) Saddle deformity caused by excessive removal of septal cartilage.

Internal

A systematic examination is essential. The inferior turbinate is very prominent and often mistaken for a polyp. Common benign nasal polyps are white/grey in colour and painless on palpation (Fig. 2.7).

Fig. 2.7 Enlarged left inferior turbinate (arrow) in a patient with rhinitis (a), compared to a patient with characteristic nasal polyps (arrow) (b).

Mucopus in the middle meatus may indicate infection in the anterior group of sinuses.

The postnasal space or nasopharynx is difficult to view with a head light and mirror. Modern flexible instruments and rigid endoscopes are ideal. The sites to visualize include the Eustachian tube cushions, the posterior choanae, the roof of the nasopharynx and the fossa of Rosenmüller, which is a recess situated immediately posterior to the Eustachian tube.

Examination of the paranasal sinuses is limited to palpation. In an acute frontal sinusitis, there is localized tenderness in the floor of the sinus. Maxillary tumours may cause expansion of the malar and deformities of the teeth-bearing alveolus.

Allergy testing

The simplest allergy test is a skin-prick performed on the volar aspect of the forearm. A wide variety of allergens may be tested, but the common ones include pollens, animal dander, and house and dust mite. Controls such as a negative control (saline) and positive control (histamine) should be employed. A positive response produces a wheal and flare (in about 20 minutes) which can be graded. A negative response does not exclude allergy, and a positive response is not absolute proof that the specific allergen is causing symptoms (Fig. 2.8). The radioallergosorbent test (RAST) measures allergen-specific serum immunoglobulin E, but is expensive.

Fig. 2.8 A skin-prick test illustrating allergy to house dust mite and grass.

Radiology

Plain X-rays of the sinuses have limited value. Computed tomography (CT) is the imaging of choice for the majority of nasal and sinus disease (Fig. 2.9). Soft tissue abnormalities and tumours require magnetic resonance imaging (MRI) (Fig. 2.10).

Fig. 2.9 CT scan showing a malignant tumour of the maxillary sinus with bone erosion in the nasal cavity and cheek.

Fig. 2.10 MRI scan (T1) complementary to Figure 2.9: soft tissue detail is enhanced.

Mucociliary clearance

Mucociliary clearance can be assessed in cases of suspected ciliary motility disorder, e.g. Kartagener’s syndrome. A pellet of saccharin placed on the anterior end of the inferior turbinate should be tasted by the patient in about 20 minutes. Prolongation of this time occurs in some normals after nasal infections and in primary ciliary dyskinesia.

Miscellaneous

Rhinomanometry and acoustic rhinometry, which measure nasal air flow/resistance and cross-sectional area, respectively, are highly specialized research tools. Nasal provocation tests are more accurate than skin tests, but are time consuming as only a single allergen can be tested at a time. Eosinophilia in nasal smears and blood is supportive of a diagnosis of allergic rhinitis.

Clinical features

The clinical features of allergic rhinitis include the classic triad of:

The symptom complex is produced by allergen binding to immunoglobulin E (IgE), which in turn is bound to mast cells. This causes degranulation of mast cells and the release of mediator substances such as histamine, leukotrienes and slow-reacting substance of anaphylaxis (SRSA).

Many patients have associated evidence of atopy such as asthma, eczema, allergic dermatitis and drug allergies. Aspirin sensitivity is not infrequent. Taking a detailed clinical history may identify the allergens involved.

Typically, the nasal mucosa has a boggy, oedematous appearance (Fig. 2.13); it is covered by a thin layer of watery secretion. Application of a vasoconstrictor produces marked mucosal shrinking with improvement in the nasal airway. Skin-prick tests should be interpreted only in relation to the history. Negative skin tests in the face of obvious allergens are not infrequent.

Fig. 2.13 Oedematous inferior turbinates narrowing the nasal airway in a patient with hay fever.

Management

The simplest treatment is avoidance of known allergens. In perennial allergic rhinitis, the quantity of dust and dust mite may be reduced in the bedclothes by:

Suspected food allergens may be excluded from the diet or replaced with suitable alternatives. Removing animal dander by giving up a pet may be emotionally upsetting but necessary.

Desensitization injections may be offered. These work on the principle of producing a blocking IgG antibody that prevents antigen binding to IgE. Obviously, the treatment is only of value if specific allergens can be identified, and it is essential to commence the series of necessary injections well in advance of the exposure. Because of the risk of anaphylaxis, desensitization must be done in a controlled environment with adequate resuscitation available. Sublingual desensitization for grass pollen allergy is also available and carries less risk.

Surgery

Surgical treatment (Fig. 2.14) is only infrequently indicated, as most patients’ symptoms are controlled by conservative therapy. Turbinate resection, cautery or outfracture may improve nasal obstruction, but rhinorrhoea and sneezing are unaffected by surgical manipulations.

Fig. 2.14 (a) Endoscopic photograph of turbinate after laser reduction; (b) resection and submucosal diathermy of inferior turbinates to relieve obstruction.

Clinical features

The main clinical features include nasal obstruction, rhinorrhoea and sneezing as in allergic rhinitis. The nasal mucosa over the inferior turbinate is congested, swollen and red, occasionally completely blocking the airway. Some patients may complain that symptoms occur on exposure to sunlight, gaseous irritants such as tobacco or with ingestion of alcohol.

Management

In all but the mildest of cases, medical treatment in the form of local and systemic decongestants should be tried. Severe cases may require submucosal diathermy, laser treatment or partial turbinectomy to clear the nasal airway (Fig. 2.14).

Management

Treatment should be prophylactic, i.e. certain preparations should only be employed as ‘short, sharp’ therapies. Established rhinitis medicamentosa requires substitution of the offending drug by one containing a steroid, or use of a systemic decongestant. In severe cases, the mucosal swelling becomes irreversible. Such cases require surgical treatment, usually partial turbinate resection (Fig. 2.14).

Antrochoanal polyp

The antrochoanal polyp is uncommon. It is usually unilateral and commences as oedematous lining in the maxillary sinus. This prolapses, usually via a posterior accessory ostium, into the nasal cavity and enlarges towards the posterior choana and nasopharynx. The patient, commonly a young adult, complains of unilateral nasal obstruction, which is worse on expiration due to the ball valve effect of the polyp in the posterior choana. If significantly large it may block both choanae and cause otological symptoms due to obstruction of the Eustachian tube (Fig. 2.16). Patients occasionally present so late that the polyp has enlarged behind the soft palate and hangs visibly in the oropharynx.

Fig. 2.16 Antrochoanal polyp. A surgical specimen showing the classic dumbbell appearance. This caused total unilateral nasal blockage.

Treatment is surgical by pernasal excision with removal of the cystic antral portion endoscopically via an antrostomy. Recurrences may require a more radical approach to the antrum to remove the roots of the cyst.

Neoplastic polyps

Neoplastic polyps (p. 110) are invariably unilateral and cause progressive symptoms: nasal obstruction, epiphora (blocking of the vasolacrimal duct), epistaxis and foul-smelling nasal discharge. They are frequently fleshy in appearance and bleed on palpation. Biopsy is mandatory.

Miscellaneous polyps

Nasal polyps are extremely rare in children. In this age group, careful consideration should be given to any evidence of cystic fibrosis, and a sweat test should be performed.

Prolapse of the meninges (meningocele) or cerebrum (encephalocele) can occur through an anterior cranial fossa defect. This should be excluded radiologically before excision or biopsy.

Rhinolith

Rhinolith is the term applied to a large foreign body found in the nose of some adults. It is composed of deposits of calcium and magnesium on a nidus such as a piece of gauze or clotted blood. There is frequently a history of nasal packing for epistaxis many years previous (Fig. 2.20).

Fig. 2.20 Rhinolith.

A large specimen extracted from a patient who had required nasal packing for epistaxis many years previous. The nidus (coloured red) was a remnant of the gauze employed.

Mandibular fractures

The common sites of mandibular fractures are shown in Figure 2.33. The weakest part of the mandible is the condylar neck; even indirect trauma may cause fractures at this site.

Fig. 2.33 (above) Mandibular fractures.

Malar fractures

Malar fractures are common and usually follow a direct blow to the cheek bone or zygoma (Fig. 2.34).

Fig. 2.34 (right) Malar fractures.

Maxillary fractures

A French doctor by the name of Le Fort described the three most common fractures of the maxillary facial bone. These have been named Le Fort I, II and III fractures (Fig. 2.35). The maxilla provides a shock-absorbing function to prevent severe damage to the skull and intracranial contents. A Le Fort I fracture line passes through the inferior wall of the antrum and allows the tooth-bearing segments of the upper jaw to move in relation to the nose. A Le Fort II allows the maxilla and the nose, as a block, to move in relation to the frontal bone and zygoma. The most severe trauma produces a Le Fort III, which separates the facial bones from the skull base.

Fig. 2.35 Maxillary fractures.

Management

These fractures require reduction and splinting for several weeks. Miniplating techniques (Fig. 2.36) have now superseded box or halo frames for many patients.

Fig. 2.36 A maxillary fracture which, after reduction, is splinted using miniplating.

Orbital blow-out fracture

Orbital blow-out fracture is usually caused by direct trauma which pushes the eye into the orbit, thus increasing the pressure in a relatively closed cavity. The weakest part of the cavity, the orbital floor, is fractured with extrusion of orbital contents into the maxillary antrum (Figs 2.37 and 2.38).

Fig. 2.37 A coronal CT scan showing an extensive orbital blow-out fracture. Notice how the soft tissue of the orbit has extruded into the roof of the maxillary antrum.

Fig. 2.38 Orbital blow-out fracture.

Nasal fractures

Nasal fractures result from either lateral or frontal forces. The former is the most common nasal injury encountered, and lateral displacements can be corrected immediately. If this is not practical, a delay of 7 days is usual to allow soft tissue swelling to subside and an accurate assessment of the deformity to be made. Reduction is performed under local or general anaesthetic and a plaster of Paris splint applied to hold the mobile fragments in position.

If the patient presents very late, so that bony union of the fragments has occurred, then cosmetic correction is feasible by performing a rhinoplasty.

Cerebrospinal fluid rhinorrhoea

A clear watery nasal discharge after facial trauma may be due to leaking of cerebrospinal fluid (CSF). The usual site of injury is the cribriform plate or posterior wall of the frontal sinus. CSF is distinguished from normal nasal secretions in a number of ways. CSF:

The diagnosis may be confirmed by the detection of fluorescein in the nose after injection via a lumbar puncture (Fig. 2.42). More recently, high-resolution CT scanning has provided a very effective way of localizing fractures (Fig. 2.43).

Fig. 2.42 Endoscopic intranasal view in a patient with traumatic CSF leak showing the green colour of fluorescein in the left olfactory area.

Fig. 2.43 A coronal CT scan showing a traumatic fracture of the right cribriform plate with prolapse of anterior cranial fossa contents.

Cavernous sinus thrombosis

Cavernous sinus thrombosis is a potentially fatal complication of infected facial wounds. It is a retrograde infection, via the facial veins, resulting in an intracranial thrombosis (Fig. 2.44).

Fig. 2.44 Cavernous sinus thrombosis. Notice how the venous drainage of the face (via the facial and ophthalmic veins) may allow retrograde spread of infection in the facial area resulting in a thrombosis of the cavernous sinus.

The condition is characterized by headaches, rigors, bilateral exophthalmos and ophthalmoplegia. High-dose parenteral antibiotics are mandatory to prevent the high mortality seen in the past.

Septal haematoma

Septal haematoma can occur as a complication of facial trauma. This condition is discussed fully on page 40.

Sensory loss

Sensory loss, producing an area of anaesthesia, is a common accompaniment of fractures of the infraorbital region with damage to the infraorbital nerve (Fig. 2.45). Post-traumatic anosmia is not an infrequent occurrence. Even relatively minor trauma may damage the delicate olfactory nerve filaments. Anosmia is invariable if the cribriform plate has been fractured. Unfortunately, there is no prospect of recovery.

Fig. 2.45 Area of sensory loss resulting from damage to the infraorbital nerve.

First-aid measures

The nostrils should be pinched together tightly and respiration continued through the mouth. A suitable container placed under the chin will catch any blood. The subject should sit upright to lower the blood pressure and lean forward so as not to swallow blood. These manoeuvres comprise ‘Trotter’s method’ for the control of epistaxis. It is useless to compress the bony root of the nose (Fig. 2.54).

Fig. 2.54 Manual compression of the nose. The technique is performed correctly in (a). No benefit is gained by attempting to apply pressure over the bony nasal pyramid (b).

If a patient presents with epistaxis in which first-aid measures have failed, and in which simple cauterization (see below) does not prevent further bleeding, hospital admission will be required for assessment of blood loss, and to identify the cause of bleeding and control the continued epistaxis.

Assessment of blood loss

A clinical assessment is made by recording the pulse and blood pressure. It is vital to appreciate that in the young an adequate blood pressure may be maintained by a rising pulse rate, but decompensation may be sudden. Other signs of shock should be looked for, e.g. pallor and sweating. An intravenous line should be inserted, blood taken for cross-matching and a suitable plasma expander commenced. A baseline haemoglobin, full blood count and clotting screen should also be requested.

Evaluation of cause

If the epistaxis has abated it is often possible to visualize the site of bleeding. This is particularly true of bleeding points in Little’s area. Examination may reveal the presence of a foreign body or a neoplastic growth. Should blood clots prevent an adequate view, the nose should be cleared by blowing. Topical anaesthesia produced by inserting cotton wool soaked in an appropriate solution will allow a greater degree of manipulation. It is wise to wear gloves, eye protectors and a gown. Suction aspiration should be to hand. If possible, an attempt should be made to determine whether the haemorrhage is arising from above the middle turbinate (internal carotid territory) or below (external carotid territory). Primary haematological disorders may be diagnosed from blood test results.

Controlling the bleeding

The precise method employed to control epistaxis is dependent on whether the bleeding has temporarily ceased, and the suspected site of haemorrhage. An obvious site of bleeding may be noted, or indicated by a surface blood clot. This may be easily dealt with by cauterization after anaesthetizing the nasal mucosa. A silver nitrate stick application is the simplest method of cauterization, but electrocautery may be employed.

A nasal pack will be required if no clear bleeding point is discernible. Traditionally, the pack consists of ribbon gauze impregnated with bismuth iodoform paraffin paste (BIPP). The nose must be cleared of clots before insertion and the pack built up in layers starting in the floor (Fig. 2.55). It is important to appreciate that, in an adult, the distance between the anterior nares and posterior choanae is upwards of 6 cm. An inflatable balloon tamponade can be used as an alternative method of packing (Fig. 2.56), or microporous sponges.

Fig. 2.55 Anterior nasal packing employing BIPP.

Fig. 2.56 Double balloon nasal packing.

Continued haemorrhage despite an anterior pack is probably due to bleeding from the posteriorly placed branches of the sphenopalatine artery and may require insertion of a postnasal pack. Specialized nasal inserts with a double balloon will allow pressure to be exerted in both the postnasal and anterior nasal spaces (Fig. 2.56). A formal gauze postnasal pack usually requires a general anaesthetic for insertion. Its dimensions should be similar to the distal phalanx of the patient’s thumb, as this compares favourably with the size of the postnasal space.

Antibiotic cover is mandatory if a postnasal pack is in situ, or if an anterior pack is left longer than 48 hours. In the elderly, it is not unusual for an acute confusional state to develop due to iodine toxicity from BIPP packs. Mild hypoxia is not uncommon after the nose is packed, and this may work synergistically with iodine toxicity.

If, despite these measures, epistaxis continues or recurs then a formal examination under anaesthetic will be needed. An obvious bleeding point may be seen endoscopically and controlled by diathermy. If not, arterial ligation of the sphenopalatine artery endoscopically, or ligation of the maxillary artery by an approach via the maxillary antrum, may be necessary (Fig. 2.57). Rarely, the external carotid artery in the neck may be ligated.

Fig. 2.57 The sphenopalatine artery can be easily accessed endoscopically by raising a mucosal flap below the attachment of the middle turbinate.

In some cases, where expertise is available, embolization of the bleeding vessel can be performed under radiological control. Small pieces of gelfoam are used to block the offending vessels.

General measures

The patient is nursed in the upright position. However, if in shock, circulation to the brain can be maintained by the head-down, feet-up posture. Carefully considered use of sedatives is useful in counteracting the anxiety which can result in a rise of blood pressure. Any hypertensive tendency will require suitable drug therapy. Specific aetiological causes such as leukaemia or neoplasia will require management once the epistaxis is controlled.

Aetiology

The majority of sinusitis is rhinogenic in origin but dental disease, facial trauma and neoplasia may be predisposing factors. As the lining of the nose is continuous with that of the paranasal sinuses, any mechanism producing rhinitis will have the potential to cause a sinusitis. The maxillary, frontal and sphenoidal sinuses drain into the nasal fossae via the ethmoid sinuses; this is important as conditions in the ethmoids and particularly in the middle nasal meatus will dictate what occurs in the remaining dependent larger sinuses. The aetiology of the rhinitis must be treated if sinus disease is to be satisfactorily managed.

Chronic sinusitis

Retained secretions allow a spectrum of bacteria to colonize the sinuses, further inhibiting clearance. The clinical features of chronic sinusitis include:

Expansion of an obstructed sinus is called a mucocele. This occurs in the ethmoid, the frontal and, uncommonly, in the sphenoid sinuses, and requires surgery.

Ethmoid sinus

Maxillary sinus

Fig. 2.65 The ostiomeatal complex. (a) This shows how the region is a common route of drainage and ventilation of the frontal, ethmoidal and maxillary sinuses. (b) Clearing the ostiomeatal complex allows enhanced ventilation and drainage of the dependent major paranasal sinuses. (c) Surgery to the ostiomeatal complex can be performed using a rigid endoscope.

Frontal sinus

Tension headaches

Tension headache is a generic term that includes headaches due to stress, disturbance of psyche and muscle contraction. They are usually episodic, but chronic symptoms can occur. The pain is bilaterally sited. The patient complains of ‘a tight band around the head’. No single specific form of treatment is satisfactory. Many patients benefit from counselling designed to reduce life’s stresses and provide emotional support. Headaches with a marked muscle component may resolve with simple massage. Drug therapy in the form of analgesics, antidepressants and sedatives in selected patients may provide some therapeutic gain.

Migrainous headaches

Migraines (Fig. 2.66) occur mainly in women and are hemicranial and paroxysmal. Prodromal eye symptoms such as halos and scotomata are not infrequent. Dilatation of intracranial vessels is the result of the disorder and in many instances can be counteracted with vasoconstrictors such as ergot preparations, beta-blockers or, for acute attacks, 5-hydroxytryptamine (5-HT) agonists.

Fig. 2.66 Comparison of migraine and cluster headaches.

Cluster headaches

Cluster headaches (Fig. 2.66) are synonymous with periodic migrainous and ciliary neuralgia. The symptoms characteristically occur in the early hours, usually in clusters with periods of relief lasting several months. Prophylactic vasoconstrictors and 5-HT agonists, such as those employed for migraine, are very effective.

Temporal arteritis

Temporal arteritis is characterized by a swollen and palpable superficial temporal artery. Visual defects progressing to blindness are a real danger. Pain symptoms are localized to the homolateral eye and temple. The diagnosis is made by showing a raised erythrocyte sedimentation rate or plasma viscosity. Urgent treatment with steroids is required on clinical grounds. If the diagnosis is in doubt, a temporal artery biopsy can be performed.

Primary neuralgias

Trigeminal neuralgia or tic douloureux can occur in any branch of the nerve. The ophthalmic division is most frequently involved and the pain can be triggered by combing the hair. Remission may last several months but relapses are frequent. Lacrimation and rhinorrhoea on the ipsilateral side are common. Most cases are helped by carbamazepine. Vascular decompression by separating an aberrant blood vessel from the intracranial portion of the trigeminal nerve has also provided relief in some cases.

Glossopharyngeal neuralgia is characterized by piercing pain in the throat, which radiates to the ear. The tonsil is the trigger zone and the pain is activated by swallowing or yawning. Carbamazepine is much less effective than in tic douloureux. Section of the glossopharyngeal nerve, either in the tonsil fossa or intracranially, has been tried with unpredictable results.

In tympanic neuralgia the site of pain is deep within the ear. Relief may be obtained by dividing the tympanic nerve in the middle ear.

Secondary neuralgias

Secondary neuralgias are produced by physical damage to nerves, usually as a consequence of compression or tumour infiltration.

An acoustic neuroma expanding in the cerebellopontine angle can cause pressure on the trigeminal and glossopharyngeal nerves. An elongated styloid process may give rise to symptoms of glossopharyngeal neuralgia by irritating the nerve as it passes the tonsil fossa (Fig. 2.67). Nasopharyngeal tumours can erode the skull base and cause invasion and compression of the trigeminal nerve.

Fig. 2.67 A lateral neck X-ray showing an elongated styloid process. This had resulted in glossopharyngeal neuralgia on the right side which resolved after excision of the process.

Postherpetic neuralgia is a frequent complication of herpes zoster infection. The ophthalmic division of the trigeminal is commonly affected. Pain may continue for several months after the vesicular rash has subsided (Fig. 2.68).

Fig. 2.68 Herpes zoster infection of the ophthalmic nerve (top) and the less frequent involvement of the maxillary nerve (bottom).

Abnormalities of the temporomandibular joint

Temporomandibular joint abnormalities are a prevalent cause of facial pain. Referred otalgia is a very common symptom in this condition (p. 13), but pain may be felt in the temple and cheek. The nerve endings in the joint are stimulated by stress due to malocclusion stretching the joint capsule. The discomfort may be noted with jaw movements, e.g. chewing. Edentulous patients are frequent sufferers. Palpation may elicit pain over the joint and crepitus may be felt and heard. Treatment consists of procedures to correct the bite and muscle relaxants to relieve associated muscular spasm.

Paranasal sinus disease

Acute sinus infection produces pain localized over the involved sinus(es) and is easily diagnosed owing to constitutional upset and the invariable presence of nasal symptoms. However, some cases of facial pain may be due to anatomical narrowing and localized disease in the middle meatus producing secondary sinus pathology in the maxillary, ethmoid and frontal sinuses (Fig. 2.70). Endoscopic surgical correction of the narrowed ostiomeatal complex will result in abolition of symptoms and restoration of normal mucosa (p. 51).

Fig. 2.70 (a) CT scan showing opaque ethmoid and maxillary antra in acute sinusitis. (b) Diagrammatic representation of the importance of the ostiomeatal complex in the drainage of the major paranasal sinuses.