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EXTENDED ANTERIOR SKULL BASE APPROACHES
there is signicant risk to critical structures or in the elderly, frail population. Malignant
tumours may also be palliated in this fashion while limiting morbidity from the resection.
Reconstruction and complications are discussed in Chapter 43.
Post-Operative Care and Tumour Surveillance
Surveillance is performed with regular endoscopic examinations and serial imaging. An
early post-operative CT or MRI scan within 3–6 months post-surgery provides a baseline that can be referenced, should the patient develop clinical features suggestive of
recurrence.
KEY POINTS
• Current evidence supports endoscopic endonasal approaches for many sinonasal
tumours.
• Thorough patient assessment and pre-operative planning is critical to success.
• Multiple approaches are available to enhance surgical visualization and tumour access.
• Safe and effective surgical plans can be formulated for the endoscopic approach to
many sinonasal tumours.
43. EXTENDED ANTERIOR SKULL BASE APPROACHES
Endonasal approaches to the ventral skull base are classied based on their orientation in
sagittal and coronal radiological planes relative to the sphenoid sinus. For large intra-cranial
tumours or malignant sinonasal tumours that involve the skull base, transfrontal, transcribriform and transplanum approaches can be combined to provide complete access to the anterior cranial fossa (Table 43.1). Lateral margins of the anterior cranial base may be extended
to the midline of the orbits by removal of the medial orbital roofs.
Sinonasal neoplasms suitable for endoscopic endonasal surgery (EES) include olfactory
neuroblastoma (aesthesioneuroblastoma), neuroendocrine carcinoma, sinonasal undierentiated carcinoma (SNUC), squamous cell carcinoma, adenocarcinoma, adenoid cystic
carcinoma and melanoma. Surgery is generally preferred as the rst treatment option for
resectable tumours that do not have a high risk of distant metastases. For tumours with
aggressive biological behaviour and increased risk of metastases (SNUC, melanoma), systemic therapy (chemotherapy, immunotherapy) is considered rst.
Table 43.1 Indications for endoscopic endonasal surgery of anterior cranial base (by surgical
approach)
Transfrontal Chronic sinusitis, mucocele, osteoma, nasal dermoid
Transcribriform Meningoencephalocele, olfactory groove meningioma, olfactory
schwannoma, olfactory neuroblastoma, sinonasal malignancy
Transplanum (suprasellar) Pituitary adenoma, craniopharyngioma, meningioma
Transsellar Pituitary adenoma, Rathke’s cleft cyst, craniopharyngioma
Supra-orbital Osteoma, meningioma, sinonasal malignancy
218 Rhinology and Facial Plastic Surgery
EXTENDED ANTERIOR SKULL BASE APPROACHES
Surgical Approaches
Transfrontal Approach
Table 43.2 Key landmarks and limits of the transfrontal approach
Key landmarks
Foramen cecum
Crista galli
Frontal sinus
Limits
Anterior: anterior table frontal sinus
Posterior: posterior table frontal sinus
Medial: crista galli
Lateral: lacrimal fossa
Superior: posterior table midpoint
Transcribriform Approach
Table 43.3 Key landmarks and limits of the transcribriform approach
Key landmarks
Crista galli
Olfactory lia, olfactory bulbs
Lateral lamella
Anterior: frontal sinus
Posterior: planum, posterior ethmoid artery
Medial: crista galli
Lateral: orbit
Transplanum Approach
Table 43.4 Key landmarks and limits of the transplanum approach
Key landmarks
Posterior ethmoid artery
Olfactory tracts
Limits
Anterior: cribriform plate
Posterior: superior intercavernous sinus
Posterolateral: optic canals
Lateral: orbital apex
Supra-Orbital Approach
Table 43.5 Key landmarks and limitations of the supra-orbital approach
Key landmarks
Anterior and posterior ethmoid arteries
Limits
Anterior: frontal sinus
Posterior: optic canal
Superolateral: midplane of orbit
Rhinology and Facial Plastic Surgery 219
EXTENDED ANTERIOR SKULL BASE APPROACHES
SUPRASELLAR APPROACH
Table 43.6 Key landmarks and limitations of the suprasellar approach
Key landmarks
Optic canals
Tuberculum
Ophthalmic arteries
Limits
Anterior: planum sphenoidale
Lateral: optic canals, paraclinoid internal carotid artery
Reconstruction
Reconstruction of dural defects of the anterior cranial base is ideally performed using vascularized tissue. Local vascularized aps include middle turbinate, inferior turbinate and
nasal septal aps, all of which are based on terminal branches of the sphenopalatine artery.
Regional vascularized aps include peri-cranial and temporoparietal fascial aps. Of these,
the nasal septal ap and extra-cranial peri-cranial ap oer the best coverage and are preferred for reconstruction of large defects of the anterior cranial base.
Dura defects (<1cm) are typically a menable to a ‘ bath plug’ type repair using fat or overlay autolo-
gous or synthetic gras. Larger defects wi ll usually require multilayer closure oen incorporating
a free-mucosal gra or vascularized ap. Very large defects (>3cm) usually require rigid reinforcement via septal cartilage or titanium mesh to minimize the risk of encephalocele formation.
Complications
Post-operatively, the most common complication is cerebrospinal uid (CSF) leak. Potential
risk factors include the size and location of the dural defect, patient factors (prior treatment,
obesity), reconstructive technique (materials, vascularized ap, packing) and peri-operative
care (patient activity, lumbar drain, debridement). In most cases, endoscopic repair supplemented by a lumbar spinal drain is successful. Intra-cranial infection is rare and is usually
associated with a post-operative CSF leak. Prompt repair of CSF leaks and limited use of
lumbar spinal drains is encouraged to limit the risk of infection.
Sinonasal complications include sinusitis, epistaxis, synechiae, chronic crusting, cosmetic
deformity and loss of olfaction. Delayed epistaxis is usually due to a branch of the sphenopalatine artery. A saddle-nose deformity can result from loss of septal support. Even if the
olfactory nerves are preserved, some loss of olfaction is common and may be due to altered
airow patterns, mucosal oedema and crusting, post-operative irradiation or direct damage
to the olfactory epithelium or olfactory tracts. Fortunately, quality of life (QoL) studies demonstrate that overall sinonasal morbidity is low.
KEY POINTS
• The anterior cranial base from the frontal sinus to the sella and from orbit to orbit is
accessible using EES.
• These techniques can be applied to a wide variety of lesions including
meningoencephaloceles, benign tumours (nasal dermoids, meningiomas,
craniopharyngiomas, pituitary adenomas) and malignant tumours (sinonasal
malignancy) with preservation of microsurgical and oncological principles.
• Many of the challenges of endonasal surgery have been solved, and large dural defects
can be reconstructed effectively using vascularized aps.
Oncological and functional outcomes are comparable or superior to other approaches
with the potential for decreased morbidity.
220 R hinolog y and Facial Plastic Surgery
GRANULOMATOUS CONDITIONS OF THE NOSE
44. GRANULOMATOUS CONDITIONS OF THE NOSE
Introduction
A granuloma is an organized collection of macrophages which fuse to form multinucleated
giant cells. is histologic conguration is encountered in a number of infective, inammatory
and neoplastic conditions of the nose and sinuses (Table 44.1) and is also seen in vasculitides.
There are often systemic manifestations, but these conditions may present with
otorhinolaryngological symptoms; a low threshold of suspicion is therefore needed for
diagnosis.
Granulomatosis with Polyangiitis (GPA)
Granulomatosis with polyangiitis (GPA; formerly Wegener’s granulomatosis) classically
involves a triad of upper airway, lung and renal disease, but limited or localized forms of
the condition occur in up to 30%. It is thought to be an autoimmune disease, associated
with cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCAs) which are specic for
proteinase-3 (PR3). Any part of the body may be aected and in generalized disease there is
oen malaise disproportionate to the clinical ndings.
GPA has been classied as
‘Localized’ (respiratory tract involvement only with no systemic vasculitis)
•
‘Early systemic’ or ‘generalized’ disease
•
Table 44.1 Granulomatous conditions of the nose and sinuses
Infective Inammatory Neoplastic
Bacteria
Tuberculosis (Mycobacterium tuberculosis) Sarcoidosis Extranodal NK/
T-cell lymphoma
Leprosy (Mycobacterium leprae) Granulomatosis with polyangiitis
(GPA, Wegener’s syndrome)
Rhinoscleroma (Klebsiella rhinoscleromatis) Eosinophilic granulomatosis
with polyangiitis (EGPA;
Churg-Strauss)
Syphilis (Treponema pallidum) Cocaine-induced midline
destructive lesion (CIMDL)
Actinomycosis (Actinomyces israelii) Giant cell granuloma
Fungal
Aspergillus (fumigatus/avus/niger) Eosinophilic granuloma
(Langerhans cell histiocytosis)
Zygomycosis (Conidiobolus coronatus,
Rhizopus oryzae)
Dermateaceae (Curvularia, Alternaria, Bipolaris)
Rhinosporidiosis (Rhinosporidiosis seeberi)
Blastomycosis (Blastomyces dermatitidis,
Cryptococcus neoformans)
Histoplasmosis (Histoplasma capsulatum)
Sporotrichosis (Sporotrichum schenckii)
Coccidiomycosis (Coccidiodes immitis)
Protozoa
Leishmaniasis (Leishmania spp.)
Rhinology and Facial Plastic Surgery 221
GRANULOMATOUS CONDITIONS OF THE NOSE
Many cases of early systemic disease progress to generalized disease, approximately 5% remain
localized.
e incidence is approximately 10–15 per million per year. e mean age at diagnosis is
40–50 years, although it can occur at any age. Men and women are equally aected. GPA is
predominantly a Caucasian disease.
Clinical Presentation
e head and neck is the most common site of involvement at presentation (73–93%). e
nose and sinuses are involved in over 80% with symptoms which include the following:
Nasal obstruction, crusting, discharge, bleeding and facial pain.
•
Destruction of the sinonasal architecture with characteristic nasal collapse (25%), sep-
•
tal perforation and ultimately the formation of a single large cavity.
One-third of patients develop otitis media with eusion.
•
Sensorineural hearing loss (35%) and facial nerve paralysis (8–10%).
•
Subglottic or upper tracheal stenosis (16%, ve times more common in childhood).
•
Oral symptoms are rare but ‘strawberry’ gingival hyperplasia is pathognomonic.
•
Ocular manifestations (50%), with visual loss in up to 8%.
•
Necrotizing vasculitis in the lungs causes cough, haemoptysis and pleuritic pain. Over
75% of patients develop renal involvement. Cutaneous manifestations include ulceration and
nodules, and both polymyalgia and polyarthritis have been described. Neurological sequelae
include meningitis, mononeuritis multiplex and cranial neuropathies.
Diagnosis
ANCA has two main staining patterns: c-ANCA, 90% of which are PR3-ANCA, and perinuclear (p-ANCA), 90% of which are myeloperoxidase (MPO)-ANCA.
c-ANCA is generally associated with systemic GPA (sensitivity 91%, specicity 99%) and
titers correlate with disease activity. However, sensitivity falls to 60% with localized disease.
Ten percent of patients with GPA have a positive p-ANCA and up to 30% may be ANCAnegative, particularly in localized disease. A full blood count, erythrocyte sedimentation
rate, C-reactive protein, renal function, serum angiotensin-converting enzyme (ACE), urinalysis and chest X-ray or chest computed tomography (CT) should be performed. Tissue
biopsy may be helpful in ANCA-negative patents. Systemic nasal biopsy shows specic features for GPA in less than 10%. e probability increases by up to 50% when deep biopsy
from major lesions is taken. Paranasal sinus biopsies yield more positive results than nasal
specimens.
CT and magnetic resonance imaging (MRI) of the sinuses may show nonspecic mucosal
thickening (90%), bony destruction (62%) and new bone formation (78%). e combination
of bone destruction and new bone formation on CT is virtually diagnostic, especially when
accompanied on MRI by a fat signal from the sclerotic sinus wall, so-called ‘tramlining’.
e American College of Rheumatology proposed a clinical classication in 1990 to distinguish GPA from other vasculitides (Table 44.2). e Chapel Hill Consensus, last updated in
2012, added PR3-ANCA to the denition in 1994.
Treatment and Prognosis
Untreated, GPA is a lethal disease with a mean survival of 5 months; a fulminating course
with a fatal outcome can occur in as little as 48 hours. e introduction of systemic corticosteroid treatment improved mortality rates to 50%. Treatment aims to induce and maintain
remission. Initial treatment typically involves steroids plus cyclophosphamide, methotrexate
or rituximab. Methotrexate, azathioprine or mycophenolate mofetil are then used as steroidsparing agents for maintenance, sometimes with co-trimoxazole.
222 R hinology and Facial Plastic Surgery
GRANULOMATOUS CONDITIONS OF THE NOSE
Table 44.2 1990 American College of Rheumatology criteria for the diagnosis of granulomatosis
with polyangiitis (GPA)*
Criteria Denition
Nasal or oral inammation Painful or painless oral ulcers or purulent or bloody nasal discharge
Abnormal chest X-ray Nodules, xed inltrates or cavities
Abnormal urinary sediment Microscopic haematuria with or without red cell casts
Granulomatous inammation
on biopsy
*
A diagnosis of GPA requires two or more of these four criteria. This rule is associated with a sensitivity of 88.2% and a specicity of 92.0%.
Granulomatous inammation within the wall of an artery or in
the peri- or extravascular area (artery or arteriole)
Topical nasal treatment such as douching, intranasal steroids and nasal lubricants may be
helpful for symptomatic relief. Surgery is generally reserved for cases that are refractory to
medical treatment, or for complications of GPA. Rhinoplasty to correct a saddle nose deformity should be deferred until the disease has been in remission for at least 1 year. Grommets
are best avoided because of the risk of chronic otorrhoea.
Eosinophilic Granulomatosis with Polyangiitis (EGPA)
is rare vasculitis of unknown aetiology, formerly known as Churg-Strauss syndrome, is
associated with chronic rhinosinusitis with nasal polyps (CRSwNP), allergic rhinitis, asthma
and eosinophilia. e mean age at diagnosis is 50 years (range 4–75 years), but there is no
gender preponderance. e annual incidence is 0.5–4 per million in Europe, rising to 67 per
million in asthmatics.
Clinical Presentation
Asthma occurs in 99% of patients and is characteristically late onset. Sinonasal symptoms
are present in up to 93%, with nasal obstruction, rhinorrhoea, anosmia, sneezing, crusting and epistaxis. Neurological symptoms are common, with mononeuritis multiplex in up
to 76% and peripheral polyneuropathy in 25%. Central nervous system involvement is less
common but is the second most common cause of death. Cutaneous symptoms including
papules and nodules occur in up to 50%. Cardiac involvement is less common but is the
major cause of mortality, usually from granulomatous myocarditis.
Diagnosis
Diagnosis is based on clinical features illustrated in Table 44.3. e condition should be
suspected in anyone with dicult-to-treat CRSwNP, asthma and a systemic eosinophilia
as the ANCA is only positive in 40–75% of cases, typically p-ANCA specic for MPO but
Table 44.3 1990 American College of Rheumatology criteria for the diagnosis of eosinophilic
granulomatosis with polyangiitis (EGPA)*
Criteria Denition
Asthma History of wheezing or diffuse rales on expiration
Eosinophilia Eosinophilia >10% on white blood cell differential count
Mononeuropathy or
polyneuropathy
Pulmonary inltrates, non-xed Migratory or transitory pulmonary inltrates on radiographs
Paranasal sinus abnormality History of acute or chronic paranasal sinus pain or
Extravascular eosinophils Biopsy including artery, arteriole or venule, showing
*
A diagnosis of EGPA requires any four or more of these six criteria. This rule is associated with a
sensitivity of 85% and a specicity of 99.7%.
Development of mononeuropathy, multiple
mononeuropathies or polyneuropathy
radiographic opacication of the paranasal sinuses
accumulations of eosinophils in extravascular areas
Rhinology and Facial Plastic Surgery 223
GRANULOMATOUS CONDITIONS OF THE NOSE
occasionally c-ANCA. Sinonasal imaging shows non-specic widespread opacication, and
patients are more likely to develop frontoethmoidal mucocoeles.
Treatment and Prognosis
Treatment is primarily with high-dose systemic steroids, but cyclophosphamide, methotrexate, azathioprine and mycophenolate mofetil may also be helpful. Remission rates are 91%
with over 25% relapse. Sinonasal symptoms should be treated with topical nasal steroids,
douching and endoscopic sinus surgery as required.
Cocaine-Induced Midline Destructive Lesion (CIMDL)
Cocaine use via intranasal inhalation is known to cause septal perforation but more aggressive midfacial destruction has also been noted. Such cocaine-induced midline destructive
lesions (CIMDLs) can mimic localized or systemic GPA as well as neoplasia.
Clinical Presentation
Patients complain of nasal obstruction and bleeding, with change in shape of the nose and
nasal regurgitation as the lesion progresses to destroy the nasal framework and palate.
Systemic symptoms are rare.
Diagnosis
Nearly 90% of patients have a positive p-ANCA against human neutrophil elastase (HNE); over
50% of patients will also have a positive PR3-ANCA. Histolog y is oen very similar to that of GPA.
Treatment and Prognosis
ere is no role for immunosuppression, and patients must stop using cocaine to prevent further progression. Conservative treatment includes nasal douching, debridement of necrotic
areas and topical or systemic antibiotic therapy.
Sarcoidosis
Sarcoidosis is a systemic granulomatous condition of unknown aetiology. It is slightly more
common in women than men with peak onset between the third and fourth decades. e incidence varies from 6–16 per 100,000 with signicant geographical variation. It is 10–20 times
more common in African Americans than Caucasians.
Clinical Presentation
Sarcoidosis primarily aects the lower respiratory tract but may involve almost any organ. It
involves the upper respiratory tract in up to 18%.
Symptomatology includes the following:
Nasal obstruction, crusting, bleeding or facial pain (1–4%).
•
Characteristic ‘strawberry skin’ appearance of nasal mucosa with or without ulcer-
•
ation, crusting, septal perforation and adhesions.
Expansion of the nasal dorsum can be associated with thickening and purplish discol-
•
oration of the overlying skin known as lupus pernio, which is a cutaneous manifestation of chronic systemic sarcoid.
Salivary gland enlargement (5–10%), which is more rarely associated with facial palsy
•
and uveitis (uveoparotid fever, Heerfordt’s syndrome).
Laryngeal involvement (1–5%), especially supraglottitis (85%), with cough, hoarse-
•
ness, dysphagia and rarely stridor.
Diagnosis
No test is pathognomonic. Diagnosis relies on a combination of clinical features, imaging,
histology, biochemical testing and the exclusion of other granulomatous diseases. e classic histological appearance is that of a non-caseating granuloma. Nasal biopsy is only helpful if the mucosa appears clinically abnormal, when over 90% of samples are positive. Serum
224 R hinolog y and Facial Plastic Surgery
DIAGNOSIS AND MANAGEMENT OF FACIAL PAIN
ACE is elevated in up to 85% during active disease, but is non-specic. Serum and urinary
calcium levels are elevated in 15%. Imaging of the chest allows staging of the disease. CT
scanning may show punctate osteolysis of the nasal bones in 25% of patients and will also
demonstrate secondary involvement of the sinuses. Bilateral lacrimal gland enlargement
may be seen.
Treatment and Prognosis
Sarcoidosis has a variable clinical course; up to two-thirds of patients will spontaneously
remit whereas 10–30% follow a chronic course despite systemic therapy.
Some patients require no treatment, but international guidelines suggest systemic or intralesional steroid treatment for life-threatening or critical disease. Hydroxychloroquine has
been used for cutaneous and sinonasal sarcoidosis. Nasal treatment includes intranasal steroids and douching. Surgery has a limited role, particularly in the presence of active disease. Septal surgery should be avoided as there is an increased rate of septal perforation.
Symptomatic laryngeal disease that fails to respond to systemic treatment may be treated
with transoral laser and intralesional steroid injection.
KEY POINTS
• Many patients with systemic granulomatous conditions present rst to ear, nose and
throat (ENT) surgeons. It is important to maintain a low threshold of suspicion to make
an early diagnosis and avert more severe systemic disease.
• Any patient with blood-stained discharge and crusting in the nose has a
granulomatous condition until proven otherwise.
• No test is completely reliable, and a combination of clinical ndings combined with
diagnostic investigations is required.
• The sensitivity and specicity of c-ANCA in GPA are 91% and 99%, respectively.
• Secondary or tertiary referral may be required to diagnose and manage the condition.
• Management should be multidisciplinary.
• A range of medications is available, of which steroids combined with cytotoxic drugs
are the most frequently used.
• Patients on long-term systemic steroids should be monitored for complications.
45. DIAGNOSIS AND MANAGEMENT OF FACIAL PAIN
Introduction
Facial pain is complex. Individuals are oen convinced their facial symptoms have an
underlying sinus aetiology. ere may be a strong psychological component and a signicant proportion of patients will have undergone unsuccessful sinus surgery. Recent
evidence showed that the majority of migraines with or without aura are diagnosed as
‘sinogenic pain’. Of patients referred to ear, nose and throat (ENT) clinic with sinogenic
pain, 80% were diagnosed with migraine and additional 8% earned the diagnosis of
migrainous headache. Dierentiating sinogenic from non-sinogenic symptoms is therefore paramount.
Sinogenic Facial Pain
Pain in sinusitis that is not acute or associated with a complication is rare (Table 45.1).
Patients may complain of pressure, fullness or throbbing in the distribution of the
Rhinology and Facial Plastic Surgery 225
DIAGNOSIS AND MANAGEMENT OF FACIAL PAIN
Table 45.1 Denitions of headache caused by rhinosinusitis and the diagnosis of rhinosinusitis
International Headache Society (IHS) denition of headache due to rhinosinusitis
(a) Any headache fullling criterion C
(b) Clinical, nasal endoscopic and/or imaging evidence of acute rhinosinusitis
(c) Evidence of causation demonstrated by at least two of the following:
• Headache has developed in temporal relation to the onset of rhinosinusitis
• Either or both of the following:
• Headache has signicantly worsened in parallel with worsening of the rhinosinusitis
• Headache has signicantly improved or resolved in parallel with improvement in or
resolution of the rhinosinusitis
• Headache is exacerbated by pressure applied over the paranasal sinuses
(d) In the case of a unilateral rhinosinusitis, headache is localised and ipsilateral to it
(e) Not better accounted for by another IHS diagnosis
Note: See EPOS2020 denition of chronic rhinosinusitis in Chapter 33.
paranasal sinuses or at the vertex of the head. Symptoms may be bilateral or unilateral
depending on which sinuses are aected. Exacerbation of these symptoms on bending
forward is not diagnostic of rhinosinusitis. Symptoms may be acute, recurrent acute
(moderated by repeated short courses of antibiotics) or chronic. ere may be associated
nasal congestion and/or hyposmia. ere should be endoscopic signs of oedema and/or
polyposis causing obstruction of outow drainage pathways, and mucosal disease. Over
80% of patients with endoscopic evidence of purulent secretions have no headache or
facial pain. If surgery is performed in cases where facial pain is the dominant symptom
without rm clinical evidence of rhinosinusitis, patients largely continue to complain of
facial pain postoperatively.
NON-SINOGENIC FACIAL PAIN
The Primary Headaches
Migraine (Paroxysmal)
Migraine is characterised by recurrent, oen unilateral, moderate to severe pulsatile or throbbing headaches lasting between 2 and 72 hours. e suerer may retreat to bed in a dark,
quiet room.
In classical migraine (25%) symptoms include:
Nausea, vomiting, photophobia.
•
Prodromal aura: a transient visual, sensory (olfaction or taste), or language or motor
•
disturbance (pins-and-needles or numbness).
60% of suerers exhibit unilateral cranial autonomic symptoms such as nasal dis-
•
charge and tearing which oen leads to confusion in diagnosis and management.
e condition runs in families in two-thirds of cases and is more common in women.
Triggers may include stress, hunger, fatigue, hormonal changes, foodstus containing tyramine (aged cheeses, smoked sh, cured meats, some types of beer), monosodium glutamate,
indoor air quality and lighting. e main aspects of treatment are trigger avoidance, acute
symptomatic control and pharmacological prevention.
Acute episodes should be treated with an oral triptan (avoid in cardiovascular disease) and
non-steroidal anti-inammatory drugs (NSAID) or paracetamol ± antiemetic. For migraine
prophylaxis, consider topiramate (risk of foetal malformations) or propranolol bearing in
mind comorbidities and side eects. If unsuitable, consider amitriptyline or acupuncture.
Botulinum toxin type A is useful in those with chronic migraines (15 or more headache days
per month of which at least 8 days are with migraines) not responding to other therapies.
Review migraine prophylaxis aer 6 months.
226 R hinolog y and Facial Plastic Surgery
DIAGNOSIS AND MANAGEMENT OF FACIAL PAIN
Tension-Type Headache (Paroxysmal or Continuous)
Usually symmetric and non-pulsatile in nature. e feeling is of tightness, pressure or constriction (vice like) that may be conned to a small area at the glabella or extend across the
whole forehead and into the temporoparietal scalp. Consider aspirin, paracetamol or NSAID
for acute treatment. For chronic tension-type headaches (continuous or last for more than
15 days per month) consider acupuncture, relaxation training, stress management and/or
counselling. Low-dose amitriptyline is also eective.
Cluster Headache (Paroxysmal)
Excruciating unilateral headaches aecting the frontotemporal and retro-orbital regions
(Figure 45.1a). Men between the ages of 20 and 50 years are most oen aected. Duration
ranges from 15 minutes to 3 hours or more, with a rapid onset and without preliminary
signs. Clusters oen continue for several weeks followed by months or years of remission.
Intense pain is caused by dilation of blood vessels creating pressure on the trigeminal nerve.
National Institute for Health and Care Excellence (NICE) recommends oxygen therapy and/
or subcutaneous or nasal triptan for acute treatment. Consider verapamil for prophylaxis
with electrocardiogram (ECG) monitoring.
Paroxysmal Hemicrania
A severe debilitating unilateral headache aecting the peri-orbital and frontotemporal
regions, with an average age of onset of 30 to 40 years. Attacks are short-lasting, ranging from 2 to 45 minutes and frequent, happening more than 5 times a day. Trigeminal
autonomic symptoms may occur. Most patients respond to indomethacin within 24 hours.
Other treatments include calcium-channel blockers, naproxen, carbamazepine, and
sumatriptan.
Trigeminal Neuralgia (Paroxysmal)
Trigeminal neuralgia is characterised by unilateral paroxysms of brief but severe pain followed by asymptomatic periods without pain, although a constant dull ache may persist in
some patients. Pain is oen described as stabbing or lancinating, burning, pressing, crushing, exploding or shooting, and patients may describe a trigger area on the face so sensitive
that touching or even air currents may trigger an episode. Vascular (arterial and venous)
compression of the trigeminal nerve roots is the likely cause in most cases. Magnetic resonance imaging (MRI) should be performed to exclude multiple sclerosis or middle fossa
pathology. Carbamazepine is the drug of choice for management. Gabapentin, lamotrigine
and topiramate are useful as second-line agents. Microvascular decompression produces satisfactory relief in most well-selected cases.
Post-Surgical/Traumatic Neuralgia (Continuous)
Post-traumatic trigeminal neuropathy often misdiagnosed as ‘sinus pain’ is related to
major maxillofacial and minor oral surgery. Third molar surgery and implants are significant contributors. The diagnosis is based on a history of surgery or trauma temporally correlated with the development of the characteristic neuropathic pain which
commonly persists 2 months after the injury and can be permanent. Medical therapy
is like that used in neuropathic pain conditions depending on the patients’ symptoms;
drugs to treat neuropathic pain (amitriptyline, gabapentin or pregabalin), infiltration
with local anesthetic and corticosteroid and, ultimately, nerve section may offer some
symptom relief.
Sluder’s Neuralgia and ‘Contact Point Pain’
e theory that implicates mucosal contact points within the nose as a cause of headache or
facial pain has, unfortunately, become rmly entrenched in otolaryngology folklore. Highquality studies now exist to support the view that the majority of people with contact points
experience no facial pain.
Rhinology and Facial Plastic Surgery 227
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