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Medicine Notes ENT Notes

Balance Disorders Notes

Updated Balance Disorders Notes

ENT Notes

ENT

Approximately 36 pages

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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,...

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