ENT Flashcards
Define Bell’s Palsy.
An acute unilateral peripheral facial nerve palsy in patients for whom physical examination and history are otherwise unremarkable, consisting of deficits affecting all facial zones equally that fully evolve within 72 hours.
Facial palsy of an otherwise known aetiology (e.g., Lyme disease-associated facial palsy), or facial palsy that is progressive, waxing and waning, or affects facial zones in an uneven fashion, is not Bell’s palsy.
Explain the aetiology / risk factors of Bell’s Palsy.
Risk factors:
- Intranasal influenza vaccination
- Pregnancy
- URTI
- Black or Hispanic ancestry
- Arid or cold climate
- Hypertension
- Family history of Bell’s Palsy
- Diabetes
Summarise the epidemiology of Bell’s Palsy.
Most population studies generally show an annual incidence of 15–30 cases per 100,000 population. Bell palsy is thought to account for approximately 60–75% of cases of acute unilateral facial paralysis, with the right side affected 63% of the time. It can also be recurrent, with a reported recurrence range of 4–14%.
Recognise the signs of Bell’s Palsy on Physical Examination.
- Unilateral (rarely bilateral)
- Involvement of all nerve branches
- Keratoconjuncitvitis sicca (dry eye) due to loss of adequate blink function (PNS dysfunction to lacrimal gland)
- Presence of risk factors
- Any age from 2 to death - peak between 15 - 45 years
Identify appropriate investigations for Bell’s Palsy and interpret the results.
Diagnosis of exclusion.
Failure to demonstrate any return of hemi-facial tone or movement within 4 to 6 months suggests an alternative diagnosis
DDx:
- Lyme disease
- Ascending inflammatory demyelinating polyneuropathy (AIDP or Guillian-Barre Syndrome)
- Sarcoidosis
- Haematogenous malignancy - e.g. leukaemia
1st Line:
- Clinical diagnosis
- Electroneuronography (ENoG) - if near-complete or complete facial paralysis (between 72hrs-14 days from onset) = >90% degrease in amplitude of compound muscle action potential (CMAP)
- Needle electromyography (EMG) - absence of voluntary motor unit potentials
- Serology for Borrelia burgdorferi - negative (Lyme disease)
2nd Line:
- Pure-tone audiometry - normal
- Tympanometry and stapedius reflex - absent or impaired reflex of ipsilateral efferent limb
- MRI - gadolinium-enhanced fine-cut of facial nerve course - post-contrast enhancement of distal meatal, labyrinthine, geniculate and tympanic/mastoid segments of facial nerve, without enlargement
- CT - fine-cut, non-enhanced = normal
Identify the possible complications of Bell’s Palsy and its management.
- Ulcerative keratitis - corneal ulcer
- Blindness
- Epiphora
- Gustatory hyperlacrimation - Bogorad’s Syndrome or crocodile tears
(Due to aberrant regeneration of pre-ganglionic PNS fibres carried within facial nerve)
Generate a management plan for Bell’s Palsy.
- Corticosteroid (Prednisolone 60mg OD oral 5 days, then reduce dose by 10mg per day after)
- Eye protection - glasses, artificial tears, ophthalmic lubricant overnight
- Concurrent anti-viral therapy - valaciclovir (500-1000mg BD oral 5-7 days), aciclovir (400mg 5 times a day oral 10 days)
- Surgical decompression
Define benign paroxysmal positional vertigo (BPPV).
A peripheral vestibular disorder that manifests as a sudden, short-lived episodes of vertigo elicited by specific head movement.
Explain the aetiology / risk factors of benign paroxysmal positional vertigo (BPPV).
Most cases result from the migration of free-floating endolymph canalith particles (thought to be displaced otoconia from the utricular otolithic membrane) into the posterior (more commonly), horizontal (less commonly), or anterior (rarely) semicircular canals, rendering them sensitive to gravity
Risk factors:
- Increasing age (>50)
- Female age
- Head trauma
- Vestibular neuronitis
- Labyrinthitis
- Migraines
- Inner ear surgery
- Meniere’s disease
Summarise the epidemiology of benign paroxysmal positional vertigo (BPPV).
One of the most common causes of vertigo.
BPPV accounted for 8% of individuals with moderate or severe dizziness/vertigo. The lifetime prevalence of BPPV was 2.4%, the 1 year prevalence was 1.6% and the 1 year incidence was 0.6%. The median duration of an episode was 2 weeks.
Recognise the presenting symptoms of benign paroxysmal positional vertigo (BPPV).
- Specific provoking positions - e.g. looking up, bending down, getting up, turning head, rolling over in bed to one side
In posterior canal BPPV, patients may identify the direction of movement that precipitates an episode, thus corresponding to the affected ear.
If vertigo is not provoked by movements, then a central disorder is considered. Labyrinthitis or vestibular neuronitis can mimic BPPV, but unlike in BPPV, head movement in any plane can precipitate vertigo that will persist for days at a time.
- Brief duration of vertigo - <30 seconds
The vertigo of other disorders lasts much longer: Meniere’s disease lasts for hours; viral labyrinthitis or vestibular neuronitis lasts for days; migraines are variable; and other central disorders can be constant.
- Episodic vertigo - over weeks to months (POSTERIOR), over days to weeks (LATERAL)
- Severe episodes of vertigo
- Sudden onset of vertigo
- Nausea, imbalance and light-headedness - can last for longer
- Absence of associated neurological or otological symptoms - more likely to be central if hearing loss, tinnitus, aural fullness
- Occurring after vestibular neuronitis and may co-exist with other conditions
Recognise the signs of benign paroxysmal positional vertigo (BPPV) on physical examination.
- Presence of risk factors
- Normal neurological examination
- Positive Dix-Hallpike manoeuvre (POSTERIOR) or positive supine lateral head turn (LATERAL)
- Normal otological examination
Identify appropriate investigations for benign paroxysmal positional vertigo (BPPV) and interpret the results.
- Dix-Hallpike manoeuvre
The patient is seated and positioned on an examination table such that the patient’s shoulders will come to rest on the top edge of the table when supine, with the head and neck extending over the edge.
The patient’s head is turned 45° towards the ear being tested. The head is supported, and then the patient is quickly lowered into the supine position with the head extending about 30° below the horizontal while remaining turned 45° towards the ear being tested. The head is held in this position and the physician checks for nystagmus. To complete the manoeuvre, the patient is returned to a seated position and the eyes are again observed for reversal nystagmus.
The Dix-Hallpike manoeuvre can also be used to diagnose the rare anterior canal variant of BPPV, but the fast phase of nystagmus would be down-beating, opposite to posterior canal BPPV of the same ear; the torsional component would be in a similar direction, although more subtle.
- Supine lateral head turns
- Audiogram
- Brain MRI
Identify appropriate investigations for benign paroxysmal positional vertigo (BPPV) and interpret the results.
- Dix-Hallpike manoeuvre
The patient is seated and positioned on an examination table such that the patient’s shoulders will come to rest on the top edge of the table when supine, with the head and neck extending over the edge.
The patient’s head is turned 45° towards the ear being tested. The head is supported, and then the patient is quickly lowered into the supine position with the head extending about 30° below the horizontal while remaining turned 45° towards the ear being tested. The head is held in this position and the physician checks for nystagmus. To complete the manoeuvre, the patient is returned to a seated position and the eyes are again observed for reversal nystagmus.
The Dix-Hallpike manoeuvre can also be used to diagnose the rare anterior canal variant of BPPV, but the fast phase of nystagmus would be down-beating, opposite to posterior canal BPPV of the same ear; the torsional component would be in a similar direction, although more subtle.
Results: Vertigo with the appropriate position-provoked nystagmus response; the nystagmus and vertigo occur with 1 to 5 seconds of latency and last <30 seconds; nystagmus is torsional (rotatory) in nature, reversible with sitting, and fatigable with repeat testing; left ear BPPV has a clockwise torsional nystagmus response, while right ear BPPV has an anti-clockwise response
- Supine lateral head turns
The clinician places the patient in a supine position and, ideally, flexes the neck 30° from horizontal to bring the lateral canals into the vertical plane of gravity. However, it is sufficient and more usual to simply lay the patient flat on his or her back.
The head is then rotated to one side, left for a minute, and then rotated to the opposite side.
Similar to the Dix-Hallpike manoeuvre, a positive test is noted when the patient experiences vertigo with nystagmus.
Results: Horizontal nystagmus without a torsional (rotatory) component; apogeotropic nystagmus (away from the ground) indicates cupulolithiasis, and geotropic (towards the ground) nystagmus indicates canalithiasis; the side with the stronger response corresponds to the affected canal in canalithiasis, and the weaker response corresponds to the affected canal in cupulolithiasis
- Audiogram - normal in primary BPPV, can be abnormal in secondary BPPV (e.g. Meniere’s & labyrinthitis = sensorineural hearing loss)
- Brain MRI - central condition finding that may mimic BPPV
Define infectious mononucleosis.
A clinical syndrome most commonly caused by Epstein-Barr virus (EBV) infection in 80-90% of cases.
Mononucleosis syndrome used when the syndrome is caused by a non-EBV aetiology.
Explain the aetiology / risk factors of infectious mononucleosis.
Risk factors:
- Kissing
- Sexual behaviour
