Showing posts with label E.N.T. Show all posts
Showing posts with label E.N.T. Show all posts

Apr 21, 2019

Broken nose | Nasal Bone Fracture aetiology and management

Definition: Fracture nasal bone (also known as Broken Nose) describes fracture of one of the bones of the nose and it is common due to many factors as described later.

Causes: Blow or accident.
Incidence: Common, due to nasal position and more common in males.

Types depend on the direction & force of trauma:
Lateral trauma: fracture at the weakest point near suture line, resulting in lateral deviation.
Anteroposterior trauma: results in either:
  • Comminution: multiple fractured bone fragments.
  • Flaring of both nasal bones over the frontal process of maxilla.
  • Telescoping of the nasal bone into the ethmoidal labyrinth, this may be associated with CSF rhinorrhea.

Symptoms of Fracture Nasal Bone

  • History of trauma
  • Pain
  • Swelling & deformity
  • Nasal obstruction
  • Epistaxis


  • Inspection: Swelling – deformity, edema.
  • Palpation: Tenderness -Crepitus.
  • Anterior rhinoscopy: septal hematoma, blood clots, mucosal lacerations.


  • X ray nasal bones lateral view: important medicolegally.

Treatment of Nasal Bone Fracture:

  • First: control epistaxis.
(A) If patient is seen shortly (within few hours) after trauma; no marked edema:
- Reduction by Walsham & Asch forceps.
- Fixation by nasal pack & external nasal splint.

(B) If there is marked edema:
Wait for 5-7 days; give antibiotics, anti-inflammatory till edema subsides, then reduction and fixation.

(C) If patient is seen late (after two weeks)
There is malunion: rhinoplasty is scheduled 3-6 months after the incident of trauma.
  • Give prophylactic antibiotics in all cases.

Key points:

The most important issues about nasal bone fracture are the timing of repair and the management of complications especially septal hematoma being the most common associated complication which may be missed if not looked for especially in comatosed patients.

Apr 16, 2019

Tinnitus definition, causes, investigations and treatment

Definition:Tinnitus is a subjective sensation of noise in the ear and / or the head, without an acoustic stimulation from outside.

Causes  and types of Tinnitus

a. Subjective: experienced by the patient only .It arises from pathological changes along the entire auditory pathway. According to the function and anatomy, the following three divisions can be made:
  1. Conductive tinnitus: Outer and middle ear pathologies.
  2. Sensorineural tinnitus: include all possible cochlear and neural (auditory nerve) pathology.
  3. Central tinnitus:
  • Primary central tinnitus,
  • Secondary central is based on the fact that conductive and sensorineural tinnitus can only be perceived as such when the peripheral signal is processed in the brain,( phantom tinnitus) .
b. Objective: tinnitus is defined as sounds originating from the body and can be heared by the patient and examiner. It may be: 

  1. Pulsatile tinnitus: is heartbeat synchronous, which is often caused by vascular abnormalities such as arteriovenous malformation, carotid stenosis, or dissections, venous sinus thrombosis, benign intracranial hypertension, and high jugular bulb or by increased blood flow (eg, in anaemia hypertension, thyrotoxicosis).
  2. Non-pulsatile tinnitus: middle-ear myoclonus (tensor tympani) , palatal myoclonus, tempro-mandibular joint (TMJ) dysfunction, patulous Eustachian tube.

Investigations for diagnosis of Tinnitus:

General: personal & occupational history, blood pressure & blood picture, Auscultation of the neck
Special: Full ENT examination, audiometry & tympanometry, and CT & MRI of temporal bone
Doppler & angiography of carotids & vertebrobasilar arteries.

Treatment of Tinnitus:

1. Specific treatment of underlying pathology.
2. Management of comorbidities e.g anxiety, depression, insomnia, decreased sound tolerance (hyperacusis). Pharmacotherapy include: anti-depressants, anti-convulsant carbamazepine, benzodiazepines.
3. IV vasodilators & plasma expanders, steroids either systemic or intratympanic.
4. In addition to other treatments:
  • Counselling and Psycho-education to help achieve habituation to the perception of the phantom sound.
  • Sound therapy, using both environmental and custom sound generators to reduce the perception of the tinnitus sound. Tinnitus Retraining Therapy (TRT) is combination of counselling and sound therapy.
  • Hearing aids for patients with tinnitus with hearing loss.

Nystagmus definition, causes, diagnosis,types, investigations

Definition: Involuntary deviation of the eyes away from the direction of the gaze followed by return of the eyes to the central resting position.

Classification and types:
a. Physiologic (optokinetic): the rapid phase is towards the center.
b. Pathologic:
  • Occular: rotatory or pendular.
  • Vestibular: has a rapid phase and a slow phase.
  • Central: vertical.

Detection and diagnosis of Nystagmus

a. Direct observation by looking into the eyes.
b. Observation using Frenzel glasses to abolish the optic fixation.
c. Electronystagmography and videonystagmography.
A. Positional testing and search for any nystagmus (central or peripheral) in:
i. Static head and body position tests (supine - head right- head left - body right - body left).
ii. Dynamic (positioning tests) for diagnosis of BPPV:
  • Dix-Hallpike test
  • Roll test.
B. Sound stimuli, the Valsalva maneuver, and tragal compression to test Tullio phenomenon
C. The Vestibulo-Ocular Reflex testing (VOR)
  • Horizontal Head impulse test (hHIT)
  •  Dynamic visual acuity test (DVA)
D. Clinical oculography test: Saccades, smooth pursuit and optokinetic testing (rotating drum test).

Vestibular investigations to diagnose Nystagmus

1. Video-nystagmography (VNG): A video of the eye that could be recorded

Caloric test:

  • The caloric test is performed with the subject reclining, head inclined 30 degree up from horizontal so as to make the lateral canal horizontal.
  • Bi-thermal caloric test stimulates the left or right ear with warm and cool air or water causing a fluid density change in the lateral canal.
  • Water is introduced into the ear canal on one side, either 7 deg centigrade above or below assumed body temperature.
  • The flow rate is such that the ear rapidly equilibrates with the water. The water is stopped after 30 seconds, and nystagmus is observed, while the subject is distracted.
  • Eye movements are usually recorded, and by comparing the response of the left and right ear to warm and cool stimuli one can determine if there is a unilateral or bilateral weakness.

Positional testing

and search for any nystagmus and determine whether central or peripheral, as in clinical testing.

Occulographic tests:

  • Saccades testing: re-fixation on new targets
  • Smooth Pursuit: tacking slow objects with foveal vision
  • Optokinetic test: sensing objects with peripheral vision

Determining the presence or absence of spontaneous or Gaze evoked nystagmus

2. Computerized dynamic Posturography (CDP):

  • Postural sway has been used as an indicator of balance function.
  • It can be recorded by force platform Posturography that measures forces needed to maintain the balance and support the body weight while standing on the platform.

3. Rotatory chair testing:

  • The rotational chair has primarily been used for analyzing horizontal canal vestibulo-ocular reflex (VOR). 
  • Angular acceleration stimulus to test VOR. Both sides are stimulated simultaneously. 
  • It is the Gold-standard test for Bilateral vestibular loss  
  • Useful to validate caloric paresis.

Other investigations:

Audiologic: PTA, Speech audiometry, Tympanometry, ABR, and OAE.
Laboratory: CBC including Hb %., blood lipid profile, Blood glucose level, Thyroid function tests, and Syphilis serology.
Radiological: -CT scan Bain, brainstem and cerebellum -MRI Bain, brainstem and cerebellum.

Apr 15, 2019

Vertigo causes, ddx, Clinical approach of diagnosis and treatment

Definition: Vertigo is a sensation of being off balance, whn you feel like you are spinning or as if the world is spinning around you.

Causes of vertigo:

  • Height vertigo 
  • Motion Sickness
  • Peripheral: Labyrinthine and vestibular nerve disorders.
  • Central: Vestibular disorders involving vestibular nuclei and their connections in the brainstem and cerebellar .

I. Peripheral

1-Benign paroxysmal positional vertigo (BPPV):
  • Very common.
  • May occur after head trauma, infection or spontaneous.
  • Recurrent attacks of severe vertigo provoked by change in head position, no deafness.
  • Due to presence of stray otoconia in the SSC.
  • A Dix-Hallpike manoever is diagnostic…..transient vertigo and nystagmus.
  • Treated by Epley manoever.
  • In resistant cases singular nerve section (the nerve supplying post. SCC).

3-Secondary endolymphatic hydrops e.g. due to Otosclerosis
5-Autoimmune inner ear disorder
6-Vascular Infarction
7-Traumatic Temporal bone fracture
  • Labyrinthine concussion 
  • Perilymphatic fistula (PLF)
-Acoustic neuroma (vestibular schwanoma) - Meningioma
  • Post-ear surgery 
  • Trans tympanic gentamycin ttt.

II. Peripheral and/or central

  • 1) Basilar migraine.
  • 2) Benign paroxysmal vertigo of childhood.
  • 3) Vestibular paroxysmia (Neuro-vascular cross-compression; disabling positional vertigo): pressure-induced dysfunction of the eighth nerve by direct pulsatile compression by arteries or rarely veins in the cerebellar pontine angle.
  • 4) Vertebro-basilar ischemia 
  • 5) AICA ischemia.

III. Central

  • 6) Vestibular epilepsy
  • 7) Paroxysmal ataxia/dysarthria (MS)
  • 8) Familial episodic ataxia
  • 9) Paroxysmal ocular tilt reaction

N.B. Some central and peripheral vestibular disorders are associated with auditory dysfunction

 Clinical approach of diagnosis and treatment of Vertigo

a. History taking

This allows differentiation of the patient’s complaint into:

  • Dizziness and light-headedness: a sensation of spatial disorientation.
  • Vertigo: abnormal sense of rotation either of the patient or the surrounding or it is a hallucination of movement.
  • Disequilibrium: off-balance, imbalance or giddiness, walking on uneven surfaces.
  • Oscillopsia: difficulty walking, riding, or reading, unable to focus on objects with movement (apparent motion of the visual scene).

Important points about history

  1. Make sure that the patient is actually describing vertigo (sense of rotation).
  2. Timing of vertigo; occurs in attacks or persistent.
  3. It should be determined whether vertigo is provoked by certain positions, as in benign positional vertigo.
  4. Associated symptoms of nausea, vomiting and diarrhea indicating the severity of vertigo.
  5. Loss of consciousness should raise the possibility of epilepsy.
  6. Symptoms of ear disease: deafness, tinnitus, earache, and discharge.
  7. Neurological symptoms: Headache, weakness, parasthesia, diplopia, ataxia and in coordination, may suggest a central cause.

b. Bedside Examination of a Dizzy Patient (clinical testing):

1. General examination: pulse B.P. for atherosclerosis, pallor for anemia.
2. Full neurological examination: including coordination, motor power, superficial and deep sensations, reflexes of UL and LL.
3. Cranial nerves examination
4. Vestibular examination:
  • Head Posture and Ocular Alignment.
  • Neurological examination: including cranial nerve testing, coordination, motor power, superficial and deep sensations, reflexes of UL and LL.
  • Balance:
Romberg test: the patient is asked to stand with the feet close together with the eyes open, and then to close the eyes. The test result is positive when the patient is stable with the eyes open but loses balance with the eyes closed.
Gait assessment (eg. Ataxic?)
Stepping test (Fukuda)

Causes of Dizziness and light-headedness (Differential diagnosis):

1-Pre-syncopal dizziness (cardiac and non-cardiac):
  • a. Orthostatic hypotension 
  • b. Cardiac arrhythmias.
2-Psychosomatic dizziness
  • a. Panic attacks 
  • b. Hyperventilation syndrome.
3-Metabolic hypoglycemia.
4-Alcohol and drug intoxication.

Apr 8, 2019

Otalgia (Earache)| causes and differential diagnosis of ear pain

Otalgia is a medical term that is used to describe ear pain or earache, and it is one of th main syptoms of ear diseases and disorders and there are many causes of otalgia.

1-Local causes

2-Referred Otalgia

To determine the cause of earache when the ear appears normal, the areas supplied by 5th, 7th, 9th, and 10th cranial nerves, and the 2nd and 3rd cervical nerves should be examined.

A. Oral cavity: (along the 5th nerve).

1. Dental carries, dental infections, un-erupted or impacted wisdom tooth.
2. Glossitis, stomatitis (particularly herpetic).
3. Malignant tumours of the tongue, and oral cavity.
4. Calculi of the parotid (wharton’s) duct.
5. Temporomandibular joint arthritis or dislocation.

B. Nose: (Along the 5th nerve).

  •  Sinusitis.
  •  Barotrauma of sinuses.
  •  Tumors of the nose and para nasal sinuses.

C. Pharynx: (Along the 9th nerve).

  • Tonsillitis, Quinsy, pharyngitis and retropharyngeal abscess.
  • Malignant tumours especially of the tonsils, hypopharynx and nasopharynx.
  • Postadenoidectomy and post tonsillectomy.

D. Larynx: (Along the 10th nerve).

  • Non specific laryngitis. - Epiglottitis.
  • T.B. Laryngitis. - Perichondritis.
  • Malignant laryngeal tumors.

E. Oesophagus: (Along the 10th nerve)

  • Forign Body. 
  •  Oesophagitis. 
  • Malignant tumors.

F. Cervical: (along the 2nd and 3rd cervical nerves).

  • Spondylosis. 
  • Osteoarthritis of cervical spine.

G. Miscellaneous:

  • Great vessel aneurysm. 
  • Acute thyroiditis.
  • Migraine. 
  • Angina pectoris. 
  • Long styloid process.


  • Trigeminal neuralgia (5th nerve).
  • Glossopharyngeal neuralgia (9th nerve).


This is diagnosed by exclusion of all other etiologies.

Apr 4, 2019

Cochlear Implants| def., components, Prerequisites and factors affecting

Definition: A cochlear implant is an electronic device that can provide useful hearing and improved communication abilities for persons who have severe to profound sensorineural hearing loss and who cannot benefit from hearing aids.

Components of Cochlear Implants

A cochlear implant has an external and internal component:
1. External component: It consists of an external speech processor and a transmitter.
2. Internal component: It is surgically implanted and comprises the receiver/stimulator package with an electrode array.

How it works?

Sound is picked up by the microphone in the speech processor. The speech processor analyses and codes sounds into electrical pulses.
The electrical impulses are sent from the processor to the transmitting coil which in turn sends the signal to the surgically implanted receiver/stimulator via radiofrequency.
The receiver/stimulator decodes the signal and transmits it to the electrode array inside the cochlea to stimulate the spiral ganglion cells. The auditory nerve is thus stimulated and sends these electrical pulses to the brain which are finally interpreted as sound.

Prerequisites of cochlear implantation:

1. Bilateral severe to profound SNHL. 
2. Little or no benefit from hearing aids.
3. No medical contraindication for surgery. 
4. Realistic expectation.
5. Good family and social support toward habilitation.
6. Adequate cognitive function to be able to use the device.

Candidates with such hearing impairment may be defined as prelingual or postlingual depending on whether they were deafened before or after the acquisition of speech.

In children who have hearing impairment at birth or early in childhood, early intervention with hearing aids or a cochlear implant is vital for auditory stimulus. Auditory deprivation, i.e. lack of auditory stimulus in the early developmental period causes degeneration in the central auditory pathways. This will limit the benefit in terms of speech and language acquisition following cochlear implantation.

Factors that predict a successful clinical outcome are:

1. Previous auditory experience (postlingual patients or prior use of hearing aids).
2. Younger age at implantation (especially for prelingual children).
3. Shorter duration of deafness.
4. Neural plasticity within the auditory system.

Hearing aid| definition, use, components and types

Definition: Sound amplification system, that increase the level of surrounding sounds to make them audible to hearing aid users.

Goals and uses of hearing aids

  1. Amplify normal speech.
  2. Hear warning signals.
  3. Help in education & language development.


1-Microphone: pick up sounds and transfer to electric energy.
2-Amplifier: amplify the electric energy.
3-Receiver: converts electric energy to sounds.
4-Power supply.
5-Controls: gain and tone control.

Types of Hearing aids

  • Air conduction: Open fit, behind the ear (BTE),in the canal hearing aid (CIC),or receiver in the ear.
  • Bone conduction hearing aid

Tests of hearing, Audiological assessment, types and result interpretation

Clinical speech testing.
The patient is asked to repeat whispered words at different intensities (other ear is masked by Barany’s box).

Tuning fork tests

Audiological assessment (Audiometery)
This is the measurement of hearing by the use of a special apparatus (audiometer) for studying the degree of hearing at different intensities and different frequencies. The resultant data are recorded as an audiogram.

  •  To detect the hearing threshold of the patient.
  •  Detect the type of hearing loss (conductive, sensorineural, or mixed).
  •  Detect the degree of hearing loss (mild, moderate, severe, or profound).
  •  Selection of a hearing aid if needed.


A- Pure tone audiometry: (PTA)

1- It is the measurement of the patient’s hearing threshold by using pure tones of a single frequency.
2- The test is done once with the ear phone to determine AC curve and once with a B.C. vibrator over the mastoid to determine B.C. curve. The hearing threshold is obtained at 8 frequencies (250, 500, 2000, 4000, 6000, 8000 HZ).

3- The hearing threshold is the minimum intensity of sound that the person can hear. Normally it varies from 0-20 dB at all frequencies.
4- The resultant two curves (A.C. curve and B.C. curve) are plotted on a graph (audiogram) and this will show the type of hearing loss.

1- Conductive hearing loss: elevated A.C. threshold, while B.C. threshold is normal (i.e. Air/bone gap).
2- Sensorineural hearing loss: Both A.C. and B.C. threshold are elevated .
3- Mixed hearing loss: Both A.C. and B.C. thresholds are elevated but with an air / bone gap (e.g. A.C. threshold is elevated more.
To determine the degree of hearing loss:
The average of A.C. threshold at 500, 1000, and 2000 HZ is obtained then the degree of hearing loss is obtained as follows:
  1.  Normal: 0 – 20 dB.
  2. Mild hearing loss: 20- 40 dB.
  3. Moderate hearing loss: 40 – 60 dB.
  4. Severe hearing loss: 60 – 80 dB.
  5. Profound hearing loss: more than 80 dB.

B- Speech audiometery

This is the hearing assessment using spoken words presented to the patient through earphones, and he is asked to repeat those words. It provides an idea about the ability to communicate:

Speech tests include:
1. Speech reception threshold (SRT)
It is the level (in dB) at which the patient can correctly repeat 50% of the presented speech material. It should match with the hearing threshold level obtained by PTA.

2. Speech discrimination
It is the percentage of the correctly repeated speech material by the patient to that presented to him. Scores of 90- 100% are normal. In SNHL it is poor than expected.
Values of speech audiometery:
-Confirms results of PTA. -Selection of a hearing aid.
-Detects malingerers. - Differentiates between cochlear and retrocochlear .

C- Impedence audiometry

(1) Tympanometry

This is the measurement of middle ear pressure, through measuring the mobility (compliance) of the T.M. :
1. Type A tympanogram: (normal)
2. Type As tympanogram: The pressure is normal but the compliance is reduced in cases of ossicular fixation as in otosclerosis.

3. Type A  tympanogram: (Hypermobile or flail)
The pressure is normal, but the compliance is increased above 1.75 mm H2O & it may exceed the limits of the machine. This occurs in ossicular disruption or dislocation.

4. Type B Tympanogram: (Flat curve) This occurs in secretory otitis media.
5. Type C Tympanogram: Normal compliance with negative pressure. This occurs in ET dysfunction.

N.B: Oscillating tympanogram occurs with glomus tumours.

(2) Acoustic reflex

Usually stapedius muscle contracts 70 – 90 dB above hearing threshold level.

D- Evoked response audiometery

This is recording of the action potentials anywhere in the auditory pathway from the cochlea up to the auditory cortex. They include:

1-Electocochleography. Diagnostic in Meniere’s disease.
2-Auditory brain stem response audiometry (ABR).
It records the electrical activity in the auditory pathway (from wave I to V.)
-Objective detection of hearing threshold level.
-Differentiates between cochlear and retrocochlear, a delay in latency of 0.4 m.sec. between the wave number V of both sides is suggestive of a retrochlear pathology (e.g. Acoustic neuroma).

3-Cortical evoked response.

E- Otoacoustic emission (OAES)

These are low intensity waves produced in the cochlear and recorded in the EAC. They are classified into:
1. Spontaneous OAES: recorded in the E.A.C. without provoking stimulus
2. Evoked OAES: recorded in response to a provoking stimulus (tones or clicks).
They are very sensitive to any cochlear abnormality and can detect and cochlear affection very early. It is used in hearing threshold detection especially in infants and children.

Psychogenic deafness and Sudden Sensory Neural Hearing Loss

 Psychogenic deafness

- Sudden deafness or unexplained fluctuation, related to emotional stress.
- Marked disparity between PTA & speech audiometry.
- Improve by psychotherapy.

Sudden SNHL:

It is an important entity, where the patient has sudden, unilateral or bilateral, partial or complete SNHL, it is either viral or vascular in origin, treated by systemic steroids, it is crucial to start treatment early to save the hearing, intratymoanic steroid injection is done if systemic steroids are contraindicated, vaso dilators and hyperbaric oxygen are also tried in an attempt to prevent permanent disabling SNHL.

Causes of Deafness in children and its effect on developement

Good hearing is important for development of language and speech, considerable hearing loss in early childhood will interfere with proper speech and the child may not be able to talk (deaf – mute).

Causes of Deafness in children 

(A) Conductive:
Mainly congenital, traumatic and inflammatory lesions e.g:
  • Ear infections (Otitis media).
  • Ototoxic (damaging the auditory system) drugs.
  • Chicken pox.
  •  Measles.
  • Mumps.
  • Head injury.
(B) Perceptive: mainly congenital, traumatic and inflammatory lesions.

Most common causes are mumps, measles, and meningitis.

How can we know that the child has suffers deafness?

Usually the child makes no reactions to loud noise and doesn't respond to mother's voice, and he makes simple sounds that taper off.

In addition, the child suffers symptoms of the disease that caused deafness e.g Otitis media, the child pulls an ears or rubs it, or cries continously without apparent reason and he may have fever.

Dec 30, 2018

Deafness definition, types and causes of hearing loss

Definition: It means diminution of hearing up to complete loss, in other words: it is total or partial inability to hear sounds.
Types: There are Organic and Hysterical causes of deafness, Organic typre is classified into 3 sub-categories as discussed below.
I. Organic: A: Conductive. B: perceptive (SNHL). C: mixed.
II. Hysterical.

A. Conductive hearing loss

It means interference of sound transmission along the conductive apparatus (External & middle ear).

I. Causes in the External Auditory Canal (EAC):

II. Causes in the Tympanic membrane:

III. Causes in the Middle Ear:

IV. Causes in Eustachian tube:

  • Congenital: cleft palate.
  • Traumatic: post adenoidectomy scarring, barotrauma.
  • Inflammatory: tubal catarrh.
  • Neoplastic: nasopharyngeal tumors.
  • Miscellaneous: hypertrophy of the adenoid.

B - Sensorineural hearing loss

It means defect in conversion of sound energy to electrical impulses (cochlea) or transfer of impulses along cochlear nerve & central connections to auditory cortex.

I. Cochlear Causes (Sensory):

a. Congenital: Hearing loss dating since birth or shortly after.

1. Hereditary due to genetic aberrations:
  • If Deafness alone:

Michael’s: total lack of inner ear development.
Mondini’s: partial aplasia of labyrinth cochlea makes 1 ½ turns.
  • If Deafness with other abnormalities:
Usher’s Syndrome: SNHL + retinitis pigmentosa.
Pendred’s Syndrom: SNHL + goitre.
Alport’s Syndrome: SNHL + nephritis.

2. Prenatal:
  • Maternal infections as rubella in the 1st trimester.
  • Drug intake in the 1st trimester e.g. quinine, aminoglycosides and salicylates.
3. Natal: (during labour): 
  • Hypoxia or anoxia of the fetus.
  • Birth trauma as in forceps delivery.
4. Postnatal:
  • Neonatal infections.
  • Erythroblastosis foetalis (Rh incompatibility).

b. Traumatic

  • Transverse fracture of temporal bone involving the labyrinth.
  • Labyrinthine membrane rupture(perilymph fistula).
  • Acoustic (noise) trauma.

c. Inflammatory (Labyrinthitis)

1- Infective:
  • Viral: measles, mumps, influenza, the deafness occurs after the febrile stage. It may be unilateral or bilateral, asymmetric and affects more the high tones.
  • Syphilitic labyrinthitis: deafness is progressive, asymmetric and may be associated with vestibular symptoms (i.e. Vertigo).
  • Bacterial: - Labyrinthitis secondary to suppurative otitis media, Meningitis: deafness is bilateral and profound.
2- Toxic:
  • Ototoxic drugs: quinine, aminoglycosides, salicylates, and Lasix.
  • Metabolic: uremia, diabetes, thyrotoxicosis.

d. Vascular

Internal auditory artery occlusion due to spasm, thrombosis or embolism.
It causes sudden hearing loss (treated by large dose of steroids).

e. Miscellaneous

  • Presbycusis (senile deafness).
  • Meniere’s disease.
  • Pure cochlear otosclerosis.
  • Perilymph fistula.

II. Retrocochlear causes

Due to lesion either in the vestibulocochlear nerve, or in the auditory pathway.

1- Vestibulocochlear nerve affection:
A- Cerebellopontine angle lesions as in acoustic neuroma, and congenital cholesteatoma.
B -Meningitis.
C-Vascular loop.

2 - Central: due to lesion anywhere in the auditory pathway. It is rare.
A-Multiple sclerosis.
B-Meningitis, encephalitis.
C- Brain tumours.
D-Cerebrovascular accidents e.g. thrombosis, haemorrhage or embolism.

C - Mixed Hearing Loss

1- Congenital meatal atresia with inner ear anomaly.
2- Fracture base of skull.
3- Complicated CSOM with labryinthitis.
4- Combined otosclerosis i.e. (footplate fixation, cochlear otosclerosis).

Acoustic Neuroma: definition, incidence, symptoms, investigations and treatment

Definition: Benign tumor arises from schwann cells of vestibular n. (vestibular schwannoma).
Incidence: 40-50 years age of presentation. 8% of brain tumors,80% of CPA.


 Arise from glial neurilemmal junction at IAM (or CPA).
Grossly: slowly growing, encapsulated, smooth, and firm.
MP: Fasiculated type (Antoni A), Reticular (Antoni B).

Clinical picture of Acoustic Neuroma

A) Otological:
  • Unilateral slowly progressive SNHL.
  • Unilateral tinnitus.
  • Vertigo is not marked as condition is slowly progressive, allows for central compensation.
B) Neurological:
  • Lost corneal reflex. 
C) Cerebellar
D) Terminal:
  • Increased intra-cranial tension and death.

Investigations for diagnosis of Acoustic Neuroma

  • PTA : reveals SNHL.
  • Speech audiogram: poorer speech discrimination than PTA (retrocochlear lesion).
  • ABR delay of wave V.
  • CT with contrast.
  • MRI with contrast: the best.

Differential diagnosis of Acoustic Neuroma

Other CPA lesions, e.g Meningioma, congenital cholesteatoma, arachnoid cyst, and pontine glioma.

Treatment of Acoustic Neuroma

  •  Surgery: approach depends on size and hearing.
  • Small intracanalicular tumor with good hearing….middle cranial fossa.
  • Large CPA tumors with good hearing……….retrosigmoid.
  • Bad hearing ….translabrynthine.
  • Gamma knife (stereotactic radio surgery).

Dec 16, 2018

Meniere’s disease| causes, symptoms, signs, diagnosis and treatment

Meniere’s disease is a disorder of vestibular labyrinth characterized by triad of paroxysmal vertigo, deafness & tinnitus due to increased volume & pressure of endolymph.
In brief: - Endolymphatic hydrops with attacks of low frequency SNHL, tinnitus, vertigo and sensation of ear fullness.

- In between attacks the patient is usually symptom free. However, the patient may present later with progressive SNHL that is detectable by audiogram even in absence of the attack.
- There’s no specific test to confirm the diagnosis. It’s usually based on the clinical findings, audiogram findings and electrocochleogram to confirm the hydrops.
- Medical treatment is the usual role. Surgery is very rarely needed and is mainly about endolymphatic sac decompression +/- shunting.

Causes of Meniere’s disease

The cause of Meniere's disease isn't understood. One popular theory that hasn't been proved is that Meniere's disease appears to be the result of the abnormal amount of fluid (endolymph) in the inner ear. Disorders that may give rise to elevated endolymphatic pressure include:
  • Metabolic disturbances.
  • Hormonal imbalance.
  • Trauma.
  • Various infections eg, otosyphilis and Cogan’s syndrome [interstitial keratitis].
  • Autoimmune diseases, such as lupus and rheumatoid arthritis, may cause an inflammatory response within the labyrinth. An autoimmune etiology was postulated after there was found to be an association with the presence of thyroid autoantibodies in patients with Meniere’s disease.
  • In addition, allergy has been implicated in many patients with difficult-to-treat Meniere’s disease. Food triggers are also important factors in the generation of hydrops.


  • Meniere’s disease appears to be more common in females than in males.
  • Meniere’s disease can be seen at almost all ages, but it usually starts between the ages of 20 and 50.
  • The female predilection of Meniere’s disease is shared with migraine headache and, in fact, there is a growing body of evidence that Meniere’s disease and migraine headache may be related and/or different spectrums of the same disease.

Clinical presentation (manifestations):

Ménière disease is defined as “recurrent, spontaneous episodic vertigo; hearing loss; aural fullness; and tinnitus. Either tinnitus or aural fullness (or both) must be present on the affected side to make the diagnosis.


  • Vertigo is a subjective sensation of motion while motionless.
  • Horizontal or rotatory nystagmus is always present during vertiginous attacks.
  • The vertiginous attacks may last from minutes to hours and often are associated with severe nausea and vomiting.
  • At least 2 definitive episodes of vertigo of at least 20 minutes duration must have occurred to make the diagnosis.
  • In 10% of patients with the symptom of vertigo, Ménière disease is the cause.
  • Between episodes, some patients are completely symptom free. Many notice progressive deterioration of hearing and balance function with each successive attack.

Hearing loss

-Sensorineural hearing loss must be documented audiometrically in the affected ear at least once during the course of the disease. There may be fluctuation in the degree of hearing loss superimposed on a gradual decrement in function.
-The hearing loss primarily affects low frequencies.


Tinnitus is often nonpulsatile and may be described as whistling, although the classic description is that of low-tone, ocean-like roaring.
- It may be continuous or intermittent, usually corresponding to the loss of hearing during the attack.


In 50%: ear fullness, otalgia & increase tinnitus.

Signs of Meniere’s disease:

- Normal tympanic membrane.
- Tuning fork: P.D.

Investigations to diagnose Meniere’s disease

1- PTA: SNHL (see above).
2- Speech audiogram: poor discrimination matching PTA.
3- Electro cochleography: diagnostic.
4- Dehydration (Glycerol) test: during the attack PTA >> 1.5 mg/kg glycerin + equal saline >> PTA after 3h.: if improved by 10-15 dB (+ve).
5- Caloric test: hypoactive labyrinth (canal paresis).
6- CT to exclude retrocochlear pathology. 


Treatment of Meniere’s disease

A. Medical ttt:

Medical therapy can be directed toward treatment of the actual symptoms of the acute attack or directed toward prophylactic prevention of the attacks. 
Most care in the emergency department (ED) is based on symptomatic relief of the clinical findings.

-Salt-restricted diet, steroids, and the use of diuretics are often first-line therapies
-Intravenous (IV) or intramuscular (IM) diazepam provides excellent vestibular suppression and antinausea effects.
-Steroids can be given for anti-inflammatory effects in the inner ear.
-IV fluid support can help prevent dehydration and replaces electrolytes.
-Typically, vestibulosuppressants and antinausea medications (eg, meclizine,
-During the quiescent phase, medical treatment of Ménière disease is tailored to each patient. 

Lifestyle and dietary changes are usually the first step. Avoiding trigger substances (eg, salt, chocolate, caffeine) alone may be sufficient. Smoking cessation also is recommended. If medications are required, a 3-month trial of a diuretic (eg, hydrochlorothiazide/triamterene) and dietary management are prescribed.

Non invasive therapies

-Rehabilitation: If the patient has balance problems between episodes of vertigo, vestibular rehabilitation therapy might improve the balance.

-Hearing aid: A hearing aid in the ear affected by Meniere's disease might improve the hearing. Doctor can refer patient to an audiologist to discuss what hearing aid options that would be best for him.

-Meniett device: For vertigo that's hard to treat, this therapy involves applying pressure to the middle ear to improve fluid exchange. A device called a Meniett pulse generator applies pulses of pressure to the ear canal through a ventilation tube.

B. Surgical ttt

-Failed prolonged medical ttt.
- Progressive hearing loss.

A) Good (serviceable) hearing.
-Intratympanic injection of selective vestibulotoxic drugs.
-Endolymphatic sac decompression (Saccus decompression).
-Selective section of vestibular nerve.

B) Bad (non serviceable) hearing.
- Surgical labyrinthectomy (not done).
- Chemical labyrinthectomy (gentamycin).

Jul 25, 2018

Bell’s palsy| definition, causes, symptoms, signs and treatment

Bell’s palsy is the most common cause of facial nerve paralysis.
Deinition: (Lower motor neuron lesion) LMNL facial palsy.

What are the causes of Bell's palsy? 

Idiopathic (several theories).
1- Vascular ischaemia: local vasospasm of vasa nervosa >> oedema of nerve sheath >> nerve compression >> secondary ischaemia & more damage. 1ry ischaemia may be due to exposure to cold draughts.
2- Viral theory: isolated viral neuritis, single manifestation of polyneuritis,or reactivation of herpes simplex.

3- Auto immune.

Incidence: The commonest cause of LMNL, 80 – 90 %.

What are the symptoms and signs of Bell's palsy?

Clinical picture of Bell's palsy

It affects mainly middle aged adults, and affects both sexes equally. It may be precipitated by exposure, to cold air draughts, emotional stress, or pregnancy. The diagnosis of Bell’s palsy is made by exclusion of all other etiologies of facial paralysis.
It presents as:

1- Unilateral LMN facial paralysis of sudden onset, which may be partial or complete, and reaches a maximum in few days.
2- Retroauricular pain may occur several hours before the onset of the paralysis.
3- A reddish chorda tympani nerve may be visible through the posterosuperior part of the T.M.
4- Metallic taste and hyperacusis.


 usually it is a clinical diagnosis
  • In prolonged,or recurrent cases CT & MRI to exclude facial neuroma.
  • To detect the level.
  • Electrodiagnostic tests.

What is the treatment of Bell's palsy?

 most cases recover spontaneously.
1- General measures.
2- Medical treatment as early as possible:
  • a) Vasodilators in 1st few hours to relieve 1ry ischaemia e.g. nicotinic acid, histamine, beta histine.
  • b) Steroids (Medical nerve decompression):

To decrease edema & inflammation.
-Should be given early in tapering dose.
-Start with prednisolone 80mg / day.
-If no response after 2w give 2nd course.
  • C) Acyclovir (Zovirax): 200 mg 5 times daily for 10 days

3- Surgical decompression
Indication: > 90% degeneration after 2weeks.
Decompression by exposing bony canal & splitting the sheath from stylo mastoid foramen to level of compression.
4- Late cases: facial rehabilitation.

Jul 11, 2018

Facial nerve paralysis| symptoms, signs, leveling, complications, management

Facial palsy is a serious disorder with serious complications.
Causes of Facial nerve paralysis are discussed in details and figures here.

Pathology of facial paralysis

1- Neurapraxia:

- Definition: Functional conduction nerve block.
- Prognosis: Spontaneous complete recovery occurs within 1 - 4 weeks.

2- Wallerian degeneration:

a) Axonotmesis:

- Definition: Degeneration of the nerve axon, but the nerve sheath remains intact.
- Prognosis: The nerve axon grows inside the nerve sheath at a rate of 1 mm/day. Spontaneous recovery occurs, but is delayed (2-3 months) and maybe incomplete.

b) Neurotmesis:

- Definition: Degeneration of the nerve axon and nerve sheath.
- Prognosis: worst. Spontaneous recovery is always incomplete and delayed up to one year.

Clinical picture of facial paralysis

Depends on site of lesion.

A. Paralysis of muscles of the face (Motor):

  1. Inability to raise eye brow (occipito frontalis).
  2. Inability to close eyes firmly (orbicularis oculi).
  3. Inability to whistle (orbicularis oris).
  4. Food collects beneath cheek (buccinator).
  5. Deviation of angle of mouth to healthy side upon smiling, drooping of angle of month on affected side, dripping of saliva & loss of nasolabial fold (levator anguli oris).

B. Sensory and parasympathetic affection

  1. Affection of GSP: decreased lacrimation.
  2. Affection of nerve to stapedius: hyperacusis (disturbed hearing).
  3. Affection of chorda tympani: metallic taste.
  • Tone: by comparing both sides at rest.
  • Power: by comparing both sides during movement.
  • Degree: partial or complete paralysis.

Differentiation between UMN and LMN paralysis:

N.B: In UMN facial paralysis only the lower half of the face is paralyzed, this is because the upper part of the motor facial nucleus supplying the upper part of the face is bilaterally represented in the cerebral cortex.

Leveling of LMN facial paralysis:

According to presentation.

Investigations to confirm diagnosis:

A- To identify the cause:

  1. CT scans of brain and petrous bone to show fractures, cholesteatoma, or tumors.
  2. MRI petrous bone to show tumors especially facial neuroma.
  3. Audiogram (PTA).

B- To detect the level of the lesion:

  1.  Schirmer’s test (test for lacrimation): It is significant when the differences between the
    lacrimal flow of both sides exceed 30% of the total bilateral lacrimation, indicating a lesion at or above the geniculate ganglion.
  2. Stapedial reflex.
  3. Taste sensation:
a- Qualitative: compare taste of different staff applied to the lateral edge of the anterior 2/3 of the tongue.
b- Quantitative: electrogustometry.

4. Submandibular salivary flow test.

C- Electrophysiological studies:

Developed to evaluate the degree of facial nerve dysfunction, and the potential for recovery, they are used only in patients with complete paralysis.
They are: minimum nerve excitability test (NET), maximal stimulation test (MST), electroneuronography (ENoG), and electromyography (EMG).
Currently the 2 most helpful are: ENoG and EMG.
  1. Nerve excitability test: Determine the minimal electrical current in milliamperes required to produce a just visible muscle contraction, and compare both side, done 3 days after injury.
  2. Electroneuronography (ENoG), evoked electromyography:
  • This is the most important test.
  • Measurement of the amplitude of the summation action potentials of the muscles when a supramaximal stimulus is applied to the nerve and compare both sides.
  • This is important to detect the percentage of degeneration, which is important to decide the way of management and prognosis.
  • It is done after 2-3 days.
3. Electromyography:
  • Fibrillation potentials indicates Wallerian degeneration.
  • Polyphasic potentials indicate regeneration, and these are detected earlier than clinical recovery.
  • Volitional activity: indicated that the nerve is in continuity.

General management of facial paralysis

1. Reassurance of the patient.
2. Care of the eyes: To prevent exposure keratitis and corneal ulceration due to lack of Bell’s phenomenon (frequent blinking):
  • Artificial tears during the day.
  • Eye ointment by night.
  • Use of sun glasses outdoors.
  • In prolonged cases, lateral tarsorraphy or gold weight implantation.
3. Care of the paralyzed facial muscles: 
To prevent disuse atrophy and fibrosis:
a- Physiotherapy and gentle massage in a circular manner.
b- Infrared heat and galvanic stimulation.
c- When voluntary movement starts, the patient should start active exercises.

4. Treatment of facial paralysis according to the cause:

5- Rehabilitation
a- Dynamic: to improve the function of the nerve during movement provided there is good status of muscles.
- End to end anastmosis of the nerve.
- Nerve graft: The cable graft is obtained from the great auricular nerve in the neck, or from the sural nerve in the leg behind the lateral meleolus.
- Cross facial anastomosis: This is an anastomosis between the facial nerves of both sides, through a supralabial tunnel, using the sural nerve.
- Hypoglosso – facial anastmosis.
b- Static: to improve the appearance of the face at rest.
   - Implantation of fascia lata slings.
   - Regional muscle transplantation e.g. temporalis muscle in the cheek.

Results of facial paralysis

1- Contractures due to fibrosis of denervated muscles.
2- Tics and spasms.
3-Cross innervation due to misdirection of the regenerating fibers, resulting in:
A-Synkinesis. B-Crocodile tears: This is lacrimation while eating.

Important causes of facial paralysis

- Bell’s palsy. -Traumatic facial paralysis. - Herpes zoster oticus. -Active otitis media.

Causes of Facial nerve paralysis, aetiology

Here is the aetiology of facial nerve palsy.

I- Supra nuclear causes (Upper Motor Neuron Lesion [UMNL]):

  • Trauma to head.
  • Meningitis, encephalitis, and abscess.
  • Brain tumors.
  • Stroke: Hge, thrombosis, embolism.

II- Peripheral causes (Lower Motor Neuron Lesion [LMNL]):

(A) Intracranial:

1) In pons: Congenital nuclear aplasia, Basal meningitis, Pontine Haemorrage, Pontine tumors, Multiple sclerosis.
2) In CPA: Congenital cholesteatoma, Meningioma, Vestibular schwannoma.

(B) Cranial (intratemporal)

1) Traumatic:
  • Birth trauma: forceps delivery.
  • Fracture especially transverse type.
  • Surgical: mastoidectomy, stapedectomy.
2) Inflammatory:
3) Neoplastic:
4) IdiopathicBell’s palsy 
The commonest cause.

(C) Extra cranial

  1. Trauma: cut wound in parotid or face surgery.
  2. Sarcoidosis of the parotid.
  3. Tumor: malignant parotid tumors

(D) Miscellaneous

  • Polyneuritis (Guillane – Barre Syndrome).
  • Diabetes mellitus.
  • Lyme disease.
  • T.B.
  • Milkersson Rosenthal Syndrome.

Jul 10, 2018

Facial nerve anatomy, course and branches

(A) Intracranial part

Facial nerve has 3 nuclei:
  1. Motor nucleus lies in pons.
  2. Superior salivatory nucleus: in pons, parasympathetic secretomotor to lacrimal, submandibular, and sublingual glands.
  3. Nucles solitarius: in medulla, sensory, carries taste sensation from the tongue.
Motor fibers form the motor root, while parasympathetic and sensory fibers join to form the sensory root (nervus intermedius).

The 2 roots emerge on the side of the brain stem, at junction between pons & medulla to cross CPA to I.A.M. Controlled by pyramidal & extrapyramidal fibers.

(B) Cranial (intratemporal) part: 


  1. Labyrinthine segment: runs in the I.A.C superior to VIII & anterior to superior vestibular nerve, runs laterally to medial wall at geniculate ganglion.
  2. Tympanic (horizontal) segment: starts at geniculate ganglion, curves to form 1st genu, runs backwards in medial wall till the posterior wall.
  3. Mastoid (vertical) segment: Runs inferiority (2nd genu), lies antero inferior to lat. SCC, then vertically downwards to leave skull at stylomastoid foramen.

(C) Extra cranial part:

Enters parotid gland >> divides into terminal motor branches.

Branches of Facial nerve

(1) In temporal bone.

a) Greater superficial petrosal: arises at geniculate ganglion >> secreto motor parasympathetic to lacrimal, nasal, palatine glands.

b) Nerve to stapedius: motor supply to stapedius.

c) Chorda tympani: exit just above stylomastoid foramen to enter ME >> carries taste from ant. 2/3 of tongue & secretomotor parasympathetic to sub lingual and sub mandibular glands.

(2) After exit from skull:

Two motor branches to stylohyoid & post belly of digastric.
Posterior auricular nerve: motor to occipital belly of occipitofrontalis.

(3) Five terminal branches in parotid:

Temporal, zygomatic, buccal, mandibular & cervical supply muscles of scalp, face, auricles & platysma.

Otosclerosis| definition, causes, incidence, types, symptoms, signs, treatment

What is Otosclerosis?

Localized hereditary disorder affecting endochondrial bone of the otic capsule, characterized by disordered bone resorption and deposition, leading to replacement of normal compact lamellar bone by abnormal spongy bone of greater thickness, cellularity & vascularity with progressive fixation of stapes.

Causes of Otosclerosis:

1- Genetic predisposition: most common among white people, uncommon among Asians, and extremely rare in black people. Estimated to occur histologically in 10% of white population, and resulted in conductive hearing loss in 1%. It is twice as common in females as in males.

- Most studies support a pattern of autosomal dominant transmission with incomplete penetrance.
- There is evidence to suggest that some cases may be related to defects in expression of the COL1A1 gene.

2- Measles.

Jul 9, 2018

Cancer of external auditory canal and middle ear | causes, diagnosis, treatment

Synonym: Malignant, Squamous cell carcinoma of middle ear and external auditory canal.
Incidence: Rare, more in males.


  1. Discharge: blood stained, foul smelling, profuse.
  2. Deafness: increased conductive deafness >> Sensory-neural hearing loss (SNHL) later.
  3. Deep seated pain.