Patients with a fractured nose present with epistaxis, bruising of the eyes and nasal bridge swelling. Initially, it is often difficult to assess if the bones are deviated, particularly if there is significant swelling. Reduction of the fracture should be undertaken in the first 2 weeks after injury and can be achieved by manipulation. However, if the fracture sets, a more formal rhinoplasty may have to be undertaken at a later stage. The patient should be examined for a head injury and the nose should also be checked for a septal haematoma. This is painful, can cause nasal obstruction, is fluctuant to touch on the nasal septum and requires immediate drainage.

Box 20.2 Types of sinusitis

Acute sinusitis	Symptoms of sinusitis lasting between 1 week and 1 month
Recurrent acute sinusitis	More than four episodes of acute sinusitis per year
Subacute sinusitis	Symptoms of sinusitis lasting between 1 and 3 months
Chronic sinusitis	Symptoms of sinusitis lasting longer than 3 months

Olfaction is mainly under the control of cranial nerve I, although irritant, unpleasant nasal sensations are carried by cranial nerves V, IX and X. Anosmia is a complete loss of the sense of smell and hyposmia is a decreased sense of smell. If odorant molecules do not reach the olfactory epithelium high in the nose, a conductive deficit of smell occurs. If the neural transmission of smell is affected then a sensorineural loss of smell is incurred. Some conditions may predispose to a mixed (conductive and sensorineural) loss of smell. The main cause of a loss of smell is nasal obstruction due to upper respiratory infection or nasal polyps. Other causes include sinonasal disease, old age, drug therapy and head injury/trauma. It is difficult to predict the speed and extent of recovery in the latter causes.

Idiopathic cases will account for many patients but before this diagnosis is accepted an assessment of the patient for the possibility of an intranasal tumour or intracranial mass should be undertaken.

For clinical purposes, and particularly in general medicine, the extreme complexity of neuroanatomy must be reduced to its core elements. The following sections cover:

• cranial nerves
• three systems of motor control:
• corticospinal or pyramidal system
• extrapyramidal system
• cerebellum
• motor unit
• reflex arc
• sensory pathways and pain
• control of the bladder and sexual function.

Table 21-4. Causes of the amnestic syndrome

Alcohol (Wernicke-Korsakoff syndrome)

Head injury (severe)

Anoxia

Posterior cerebral artery occlusion (bilateral)

Herpes simplex encephalitis

Chronic sedative and solvent abuse

Bilateral invasive tumours

Arsenic poisoning

Following hypoglycaemia

The ear can be divided into three parts: outer, middle and inner.
The outer ear has a skin-lined tube 2.5 cm long leading down to the tympanic membrane (the ear drum). Its outer third is cartilaginous and contains hair, sebaceous and ceruminous glands, but the walls of the inner two-thirds are bony. The outer ear is self-cleaning as the skin is migratory and there are no indications to use cotton wool buds. Wax should only be seen in the outer third.

The middle ear is an air-containing cavity derived from the branchial clefts. It communicates with the mastoid air cells superiorly, and the Eustachian tube connects it to the nasopharynx medially. The Eustachian tube ventilates the middle ear and maintains equal air pressure across the tympanic membrane. It is normally closed but opens via the action of the palatal muscles to allow air entry when swallowing or yawning. A defect in this mechanism, such as with a cleft palate, will prevent air entering the middle ear cleft which may then fill with fluid. Lying within the middle ear cavity are the three ossicles (malleus, incus and stapes) that transmit sound from the tympanic membrane to the inner ear. On the medial wall of the cavity is the horizontal segment of the facial nerve, which may be damaged during surgery or by direct extension of infection in the middle ear.

The inner ear contains the cochlea for hearing and the vestibule and semicircular canals for balance. There is a semicircular canal arranged in each body plane and these are stimulated by rotatory movement. The facial, cochlear and vestibular nerves emerge from the inner ear and run through the internal acoustic meatus to the brainstem

The ossicles, in the middle ear, transmit sound waves from the tympanic membrane to the cochlea. They amplify the waves by about 18-fold to compensate for the loss of sound waves moving from the air-filled middle ear to the fluid-filled cochlea. Hair cells in the basilar membrane of the cochlea detect the vibrations and transduce these into nerve impulses which pass to the cochlear nucleus and then eventually to the superior olivary nuclei of both sides; thus lesions central to the cochlear nucleus do not cause unilateral hearing loss.
If the ossicles are diseased, sound can also reach the cochlea by vibration of the temporal bone (bone conduction).

EXAMINATION

The pinna and postauricular region should first be examined for scars or swellings. An auroscope is used to examine the external ear canal whilst the pinna is retracted backwards and upwards to straighten the canal. Look for wax, discharge or foreign bodies. The tympanic membrane should always be seen with a light reflex anteroinferiorly. Previous repeated infections may cause a thickened, whitish drum but fluid in the middle ear may show as dullness of the drum. Perforations are marginal or central.

COMMON DISORDERS

The discharging ear (otorrhoea)

Discharge from the ear is usually due to infection of the outer or middle ear.
Otitis externa is a diffuse inflammation of the skin of the ear canal. The organism may be bacterial, viral or fungal and the patient usually complains of severe pain. Gentle pulling of the pinna is tender and there may be lymphadenopathy of the preauricular nodes.
Examination may reveal debris in the canal which needs to be removed either by gentle mopping or preferably by suction viewed directly under a microscope. In severe cases the canal may be swollen and a view of the tympanic membrane impossible. Any foreign body seen should be removed with great care by trained personnel.

Treatment is with regular cleansing and topical antibiotics combined with corticosteroids; it resolves in 3-4 days.
Otitis media can also present with discharge from the middle ear through a perforation of the tympanic membrane. There are no mucous glands in the external ear canal, however, and if the discharge is serous then middle ear pathology is unlikely.
Treatment is with systemic antibiotics.

Cholesteatoma

Cholesteatoma is defined as keratinizing squamous epithelium within the middle ear cleft and can present with foul smelling otorrhoea. Examination may show a defect in the tympanic membrane full of white cheesy material. Mastoid surgery is required to remove this sac of squamous debris as it can erode local structures such as the facial nerve or even extend intracranially.
Hearing loss

Hearing loss:

- Type Defect Rinne Weber
- Conductive Outer or middle ear Negative Sound heard louder on the affected side
- Sensorineural Inner ear or more centrally Positive Sound heard louder in the normal ear

Deafness can be conductive or sensorineural and these can be differentiated by the Rinne and the Weber tests

Rinne test

Normally a tuning fork, 512 Hz, will be heard as louder if held next to the ear (air conduction) compared to being placed on the mastoid bone (Rinne positive). If the tuning fork is perceived louder when placed on the mastoid (bone conduction), then a defect in the conducting mechanism of the external or middle ear is present (Rinne negative).

Weber test

A tuning fork placed on the bridge of the nose of a patient with normal hearing (or with symmetrical hearing loss) should be perceived centrally.

Conductive hearing loss may be due to many causes but wax is the commonest.

Perforated tympanic membrane

This may arise from trauma or chronic middle ear disease where recurrent infection results in a permanent defect. Surgical repair is only indicated if the patient is symptomatic with hearing loss or recurrent discharge.

This is an acute inflammation of the middle ear, causing severe pain (otalgia) and conductive hearing loss. This occurs because fluid accumulation in the middle ear impairs sound conduction to the cochlea. It is often viral in origin, e.g. following a cold, and will settle within 72 hours without antibacterial treatment. In patients with systemic features or after 72 hours, a systemic antibiotic, e.g. amoxicillin, should be given. Topical therapy is of no value. Complications include infection of the mastoid bone.
Acute otitis media may spread to the mastoid area and if there is tenderness and swelling over the mastoid then an urgent ENT opinion should be obtained.

Secretory otitis media with effusion (also called serous otitis media or glue ear)

This is common in children because of Eustachian tube dysfunction. The effusion resolves naturally in the majority of cases but can persist giving hearing loss, and it predisposes to recurrent attacks of acute otitis media. A grommet is a tube that is inserted into the tympanic membrane and ventilates the middle ear cavity, i.e. it takes over the Eustachian tube’s function. Grommets are extruded from the tympanic membrane as it heals (lasting from 6 months to 2 years) but if the Eustachian tube is still not working, fluid will reaccumulate in the middle ear cavity with a return of symptoms. In most children the middle third of the face grows around the age of 7-14 years and Eustachian tube dysfunction is rare after this.

Otosclerosis

This is usually a hereditary disorder where new bony deposits occur within the derivatives of the otic capsule, specifically the stapes footplate and in the cochlea. Characteristically seen in the second and third decades, it is commoner in females and can become worse during pregnancy. The hearing loss may be mixed, and treatment includes a hearing aid or replacement of the fixed stapes with a prosthesis (stapedectomy).

This is the commonest cause of deafness. It is a degenerative disorder of the cochlea and is seen in old age. The onset is gradual and the higher frequencies are affected most (Fig. 20.3). Speech has two components: low frequencies (vowels) and high frequencies (consonants). When the consonants are lost, speech loses its intelligibility. Increasing the volume merely increases the low frequencies and the characteristic response of ‘Don’t shout. I’m not deaf!’ A high-frequency-specific hearing aid will do much to ease the frustrations of both the patients and their close contacts.

Noise trauma

Cochlear damage can occur, for example, when shooting without ear protectors or from industrial noise (see p. 1030) and characteristically has a loss at 4 kHz.

Acoustic neuroma

This is a slow-growing benign Schwannoma of the vestibular nerve which can present with progressive sensorineural hearing loss. Any patient with an asymmetric sensorineural hearing loss should be investigated, e.g. with an MRI scan.

Vertigo

Vertigo is usually rotatory when it arises from the ear. The presence of otalgia, otorrhoea, tinnitus or hearing loss suggests an otologic aetiology. Vestibular causes can be classified according to the duration of the vertigo:
seconds to minutes – benign paroxysmal positional vertigo (BPPV)
minutes to hours – Ménière’s disease
hours to days – labyrinthine or central pathology.

Benign paroxysmal positional vertigo (BPPV)

BPPV is thought to be due to loose otoliths in the semicircular canals, commonly the posterior canal. Positional vertigo is precipitated by head movements, usually to a particular position, and may occur when turning in bed or on sitting up. The onset is typically sudden and distressing. The vertigo lasts seconds or minutes and the phenomenon becomes less severe on repeated movements (fatigue). There is no serious underlying cause but it sometimes follows vestibular neuronitis (p. 1190), head injury or ear infection.

Diagnosis

This is made not only on the history but by precipitating an attack by carrying out a positional test in the outpatient clinic. This test, called the Hallpike manoeuvre, involves sitting the patient on a couch and then turning the patient’s head towards the affected ear. The patient’s head is supported by the examiner and the patient then lies down so that the head is just below the horizontal. Nystagmus (following a latent interval of a few seconds) is noted, as is any subjective sensation of vertigo. A positive Hallpike test confirms BPPV, which can be cured in over 90% of cases by the Epley manoeuvre. This involves gentle but specific manipulation and rotation of the patient’s head to shift the loose otoliths from the semicircular canals.

A differential diagnosis is a cerebellar mass but here, positional nystagmus (and vertigo) is immediately apparent (no latent interval) and does not fatigue.

Ménière’s disease

This condition is characterized by recurring episodic rotatory vertigo lasting 30 minutes to a few hours; attacks are recurrent over months or years. Classically it is associated with a low frequency sensorineural hearing loss, feeling of fullness in the affected ear, loss of balance, tinnitus and vomiting. There is a build-up of endolymphatic fluid in the inner ear, although its precise aetiology is still unclear.

Treatment involves the use of vestibular sedatives, e.g. cinnarizine in the acute phase, low-salt diet, betahistine, and avoidance of caffeine. If the disease cannot be controlled in this way, then a chemical labyrinthectomy, which involves perfusing the round window orifice with ototoxic drugs such as gentamicin is possible. Gentamicin destroys the vestibular epithelium; therefore the patient has severe vertigo for around 2 weeks until the body compensates for the lack of vestibular input on that side. The patient will happily trade occasional mild vertigo when the balance system is challenged to the unpredictable, severe and disabling attacks of vertigo of Ménière’s disease.

Labyrinthine or central causes of vertigo

These are managed with vestibular sedatives in the acute phase. Most patients will settle over a few days but continuous true vertigo with nystagmus suggests a central lesion. A patient with a deficit of vestibular function due to viral labyrinthitis or neuronitis should be able to come off the vestibular sedatives within 2 weeks, as long-term use can give parkinsonian side-effects, delay central compensation and thus prolong the vertigo. Vestibular rehabilitation by a physiotherapist or audiological scientist can speed up the compensation process, although most patients will be able to do this themselves with time.

Tinnitus

This is a sensation of a sound when there is no auditory stimulus. It can occur without hearing loss. Patients describe a hissing or ringing in their ears and this can cause much distress. It usually does not have a serious cause but vascular malformation, e.g. aneurysms, or vascular tumours may be associated.
Tinnitus associated with deafness is described above.

Treatment

This is difficult. A tinnitus masker (a mechanically produced continuous soft sound) can help. A vestibular sedative, betahistine, is occasionally used.