#12130 - Balance Disorders - ENT

Balance Disorders

Vertigo = illusion of movement

• Normal balance requires

  • Accurate sensory information from

    • Eyes (vision)

    • Proprioceptive receptors

    • Vestibular labyrinth

  • Co-ordination of information in brain

  • Normal motor output from CNS to intact musculoskeletal system

A fault in any of the above impairs balance

• Vertigo is always a symptom of vestibular defects

  • Severe if accompanied by nausea and vomiting

• Can be caused by

  • Peripheral vestibular disorders (BPPV, Menieres’, labrynthitis)

  • Spread of infection from middle ear disease to labyrinth

  • Central vestibular disorders e.g MS, tumours, infarcts

  • External insults by drugs, anaemia, hypoglycaemia etc

Benign Paroxysmal Positional Vertigo (BPPV)

Commonest cause of vertigo

Pathophysiology

• Detachment of otoconia (calcium carbonate crystals) from the otolith organ of the utricle – fall into posterior semicircular canal (loose inside canal)

• Cause symptoms on movement of the head

Aetiology

• Head injury

• Viral infection

• Degenerative changes with aging

• Idiopathic

Clinical features

• Episodic attacks or vertigo provoked by head movements e.g rolling over in bed/looking upwards

• Violent symptoms but last only seconds

• No auditory symptoms

• Episodes usually last for several months before disappearing but often recur

• Both labyrinths may be affected

Management

• Reassurance, advice to avoid provoking head position until recovery

• Avoid alcohol

• Epley maneuvers may help reposition otoconia away from the posterior canal

• Medication

  • Betahistine

  • Vestibular sedatives e.g prochlorperazine

  • Antidepressants

• Last resort = posterior semicircular canal denervation/obliteration

Meniere’s Disease

A disorder of endolymph control

Pathophysiology

• Expansion of endolymph spaces (endolymphatic hydrops) = increased fluid

• Increased pressure causes rupture of inner ear membranes

• Endolymph + perilymph mix

• Causes biochemical disturbance leading to acute vestibule-cochlear failure

Aetiology

• Idiopathic

Clinical features

• Usually unilateral

• Occurs in those aged 30-60yrs

• Triad of symptoms

  • Vertigo

  • Hearing loss

  • Tinnitus

• Attacks occur in clusters with periods of remission

• Each attack lasts several hours

• Can be accompanied by N+V

• May have warning symptoms before and attack e.g sensation of pressure in the ear, change in character of tinnitus, pain in the neck or increased deafness

• Accompanying deafness = sensorineural

  • Fluctuates in severity

  • Improves on remission

  • Associated with speech distortion

  • Discomfort with loud noises (hyperacusis)

  • Over time gradually deteriorates

• Tinnitus = roaring, low pitched, worse when hearing is most impaired

Management

• Acute

  • Cyclizine

• Medical

  • Vasodilators e.g betahistine

  • Nicotinic acid

  • Diuretic + salt restricted diet (electrolyte imbalance theory)

• Surgical

  • If symptoms not controlled by medication

  • Decompress endolymphatic sac

  • Selective division of vestibular branch of vestibularcochlear nerve

  • Labyrinthectomy = guarantees relief from vertigo but at the expense of total hearing loss in that ear

Labyrinthitis/Sudden vestibular failure

Pathogenesis

• One peripheral labyrinth suddenly stops working

• Can be due to viral infection, head injuries, blockage of end artery supplying the labyrinth, MS, diabetic neuropathy

Clinical features

• Rapid onset

• Sudden vertigo which persists continuously for days-weeks before improving

  • May be exacerbated by head movements

• N+V

• No auditory symptoms

  • Unless cochlear is involved

• Nystagmus

• Patients gradually regain balance

• Recovery slower and less complete in elderly

Acoustic Neuroma (vestibular schwanomas)

• Develop on superior vestibular nerve

• Are tumours from schwann cells

• Arise from defect on the long arm of cr 22

• Rarely become malignant (although with continued growth can compress brainstem = death)

• Can be part of an unpleasant syndrome “neurofibromatosis type 2”

  • Autosomal dominant, presents in youth, bilateral acoustic neuromas

• 50% of more do not grow in a 10yr period

• Some grow erratically + relentlessly while other never grow beyond size at diagnosis

Clinical features

• Often none

• Some present with minor ontological symptoms

• Others present with major neurological problems

Diagnosis

• ENT, cranial nerve and cerebellar examinations

• Audiogram

• MRI shows tumour

Management

• Removal of tumour and shunt (if caused raised ICP + brainstem compression)

• Watch and wait (small tumours, no neuro symptoms)

• Stereotactic radiotherapy (different directional beams focused on tumour = reduces damage to surrounding structures)

Assessment of vertigo

• Symptom recognition

• Don’t want to miss destructive middle ear disease or central vestibular abnormalities

• Examine CNS, CVS + ears

• Exclude cholesteatoma by visualizing tympanic membrane

• Spontaneous jerk nystagmus always a sign of vestibular disease

  • Indications of central causes of nystagmus include

    • Nystagmus persisting > weeks

    • Change in direction of beat (either with time or direction of gaze)

    • Non-horizontal beating or different jerks in the two eyes

• Observe the patient walking heel-toe

Romberg’s test

• Tests for proprioceptive dysfunction

• Ask patient to stand with feet together and then close their eyes

• If the patient requires vision in order to stand steadily = Romberg’s positive

Unterberger’s test

• Identifies which labyrinth may be dysfunctional in a peripheral vertigo

• Ask patient to undertake stationary stepping for 1 minute with eyes closed

• A positive test is indicated by rotational movement of patient towards side of the lesion

Hallpike maneuver ...