Vertigo Module Overview

15 March 2016 Articles 6636
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Target Audience: This module aims to convey the basic concepts of managing patients with vertigo and can be completed within a flexible timeframe. It has been designed with continuous professional development in mind and aims to reach medical practitioners, Basic Surgical Trainees and clinical medical students in their final years.

CONTENTS

 

  • Prevalence of Dizziness
  • Physiology
  • Anatomy
  • Definition of vertigo
  • Aetiology
  • Commoner peripheral vestibular disorders
  • Symptom evolution
  • History
  • Examination
  • Investigations
  • References

 

 

P  R  E  V  A  L  E  N  C  E    O  F   D  I  Z  Z  I  N  E  S  S

Dizziness is an important symptom affecting up to one-third of population by age 651. Balance problems are the primary factors that lead to falls in the elderly2. In the elderly, neural degeneration, vascular insufficiency and deterioration of vision contribute to a gradual deterioration of balance. Indeed, some areas in the UK have, for some years now, provided a specialized fall service, where clinicians with appropriate skills evaluate older patients presenting with recurrent falls.

Patients with vestibular dysfunction are prone to develop anxiety symptoms, including agoraphobia. In a survey of 3884 people recruited from general practitioner’s lists 262 individuals in the community had significant dizziness. Although the physical disorder may be mild, it is typically accompanied by a psychiatric disturbance3.

 

P  H  Y  S  I  O  L  O  G  Y

The balance system may be thought of as a reflex with a sensory input on one side consisting of the inner ear organs, proprioception sensation and ocular input. These ‘inputs’ supply information to a central processing area, the brainstem, particularly the vestibular nuclei. After integration and modification of information in conjunction with the cerebellum and cerebrum the ‘output’ part of the reflex arc then modifies posture to maintain the stability of the body and the direction of gaze.

The vestibular labyrinth in the inner ear detects linear and angular acceleration of the head. The eyes obtain information of the surroundings and about head movements, besides defining the horizon. Touch and pressure receptors in the skin, joints and muscle spindles, which are especially abundant in the neck muscles detect the relationship of the various parts of the body to each other.

In the event that input from the labyrinth to the processing center is reduced or disordered, the patient attempts to amplify other inputs by gripping onto (to augment proprioceptive input) or by fixating onto stationary objects (to augment visual input). (See Fig 1)

 

 

 

 

A  N  A  T  O  M  Y  -  B  r  i  e  f     o  u  t  l  i  n  e

The delicate membranous structures of the vestibular labyrinth are filled with endolymph, a fluid high in potassium and low in sodium. An active ionic pump keeps this fluid separate from the surrounding perilymph, in which the membranes are bathed.

The vestibular labyrinth is made up of three semicircular canals at right angles to each other. The suprerior, posterior and lateral canals have five ends since the superior and posterior canals join at one end to form a common canal. (See Fig 2The five ends open into the utricle.

 

 

 

At one end of each canal is a dilated portion, the ampulla, containing a specialized saddle-shaped neuroepithelial structure, the crista. The crista detects angular acceleration. The utricle and a neighbouring similar dilatation in the membranous labyrinth, the saccule, each contain a flat neurosensory structure. These so-called maculae are set at right angles to each other and detect linear acceleration. Embedded in a gelatinous membrane overlying the maculae are many calcium carbonate crystals, the otoconia.

On head movement, fluid inertia causes deflection and stimulation of sensory neuroepithelium.

D  E  F  I  N  I  T  I  O  N     O  F    V  E  R  T  I  G  O

Patients present with ‘dizziness’ a lay term meaning sense of disorientation. Vertigo is a hallucination of movement, that is, a sense of unreal movement.

Dizziness may encompass several different sensations such as unsteadiness, lightheadedness and giddiness. Frequently, patients have more than one type of sensation. This is compounded by the fact that the aetiology in a dizzy patient may be multifactorial.

A  E T   I  O  L  O  G  Y  :    C  A  U  S  E  S     O  F   D  I  Z  Z  I  N  E  S  S

Dizziness consists of various entities and it is difficult to quantify true prevalence in the primary healthcare setting. Sloane et al4 reported a prevalence ranging from 1.8% in young adults to over 30% in the elderly.

Studies looking at dizzy patients seen at tertiary referral centers have given an indication of what the specialists have diagnosed. Baloh et alexamined 103 elderly dizzy patients and identified benign paroxysmal positional vertigo (BPPV) and cerebrovascular disorders as the most common diagnoses. Sekine et alin their review of 626 patients attending a University Hospital, listed the main diagnoses of dizzy patients as BPPV (32%), Meniere’s disease (12%), other peripheral vestibular disorders 20%, orthostatic hypotension (4%), central vestibular disorders, including posterior fossa tumours (7%), cerebral infarction (2%).

The commonest causes of dizziness therefore include:

  • Otological-Meniere’s disease, Benign paroxysmal positional vertigo (BPPV), Vestibular neuronitis, labyrinthitis, Acoustic Neuroma (schwannoma of vestibular nerve), drug-induced, autoimmune, Chronic suppurative Otitis Media, Otitis Media with Effusion, wax, trauma to temporal bone in head injuries, Herpes Zoster Oticus (Ramsay-Hunt Syndrome), temperature changes in open mastoid cavities of patients having suction clearance
  • Cardiovascular: eg dysrythmias, hypotension (postural), embolic phenomena
  • Neurological (migraine, epilepsy, syncope, infective, vascular including vertebrobasilar insufficiency, tumours, Multiple Sclerosis and other demyelinating disorders, psychogenic)
  • Drug-induced (eg aminoglycosides)
  • Metabolic-eg, hypoglycaemia, hyperprolactinaemia

 

C O M M O N   V E S T I B U L A R    C O N D I T I O N S

Viral labyrinthitis

Labyrinthitis is an inflammatory process affecting the labyrinths that house the vestibular system of the inner ear. It usually follows an upper respiratory tract infection, where viruses spread to the labyrinth via the blood stream. Labyrinthitis causes vertigo and nystagmus with the fast phase beating away from affected ear. Cochlear symptoms such as tinnitus and hearing loss may be present in the infected ear. Nausea, anxiety and a general ill feeling are common due to the distorted balance signals that the cerebrum receives from the labyrinth. Labyrinthitis may be caused by a virus (such as the the herpes virus) but can also arise from bacterial infection (a sequel to otitis media, both acute and chronic) or head injury (compound fractures of the temporal bone). Viral labyrinthitis damages neuroepithelial structures such as the maculae and auditory hair cells, and causes permanent vestibular and possibly, hearing loss.

Vertigo and nystagmus last 3-5 days with a gradual spontaneous resolution of symptoms. Prochlorperazine is commonly prescribed for all types of labyrinthitis, and helps symptomatically. 

Recovery from acute labyrinthitis by means of central compensation generally takes from one to six weeks. However it is not uncommon for residual dizziness to last for many months or even years, especially in patients who are diabetic or hypertensive.

 

Benign Paroxysmal Positional Vertigo (BPPV)

Two main theories have been put forward to explain the clinical findings in BPPV.

In the canalolithiasis theory otoliths that have detached from the maculae float freely in the endolymph of the semicircular canal (Fig 3). As they fall through the canal on head movement the drag of fluid behind them causes displacement of the cupula with hair cell displacement and stimulation of the VOR. The particles have to fall some distance before this movement is set up, hence the latency for the appearance of symptoms and nystagmus.

In the cupulolithiasis theory, particles are thought to be adherent to the cupula of the crista ampullaris cause amplified movement and stimulation of neurosensory epithelium with sensation of vertigo. Cupulolith particles reside in the ampulla of the SCCs and are not free floating.

Both these mechanisms may coexist.

BPPV is one of the commonest causes of vertigo. The incidence of BPPV increases with age and is more common in women. By age seventy, 30% of the elderly have had at least one episode. BPPV is also associated with head trauma. The posterior canal is involved in 80% of cases. Patients typically report a brief spell of rotary vertigo on rolling in bed (onto the bad ear) or when looking up and back7.

The modern management of BPPV is by particle repositioning manoevers8, 9.


 

Vestibular neuronitis

Vestibular neuronitis is an acute, sustained dysfunction of the peripheral vestibular system with secondary nausea, vomiting, and vertigo. As this condition is not clearly inflammatory in nature, neurologists often refer to it as vestibular neuropathy.

Its aetiology remains unknown, yet vestibular neuronitis appears to be a sudden disruption of afferent neuronal input from one labyrinth. This imbalance in vestibular input to the central nervous system (CNS) causes symptoms of severe vertigo lasting several weeks. Vertigo gets worse with movement so the patient is confined to bed. The age of onset is around the fifth decade. Spontaneous horizontal nystagmus with the fast phase beating towards the opposite ear is the main sign. There is no hearing loss or other CNS signs (eg neck rigidity, fever, cranial nerve palsies, truncal ataxia, multidirectional nystagmus)

The condition resolves spontaneously with central compensation.

 

Meniere’s disease

Meniere’s disease is idiopathic endolymphatic hydrops. The incidence of Meniere’s disease is approx 1-2/10,000. It is diagnosed mainly from the history and runs its course over several years. A group of symptoms should be present, that is, the patient should have episodic tinnitus, hearing loss and vertigo. American Acadamy criteria (AAA-HNS) include

  • At least two episodes of spontaneous rotational vertigo lasting at least 20min to several hours
  • Fluctuating but audiometrically documented hearing loss; at least 10dB; initially low-tone
  • Tinnitus or aural fullness (not always present) The course of the illness is characterised by fluctuating hearing and over time the loss is progressive.

Meniere’s disease is symptomatically treated by a variety of drugs including betahistine, cinnarizine, prochloperazine, steroids, diuretics and aminoglycosides (systemically and topically in the middle ear). Surgical treatment may include decompression of the endolymphatic sac or plugging of the semicircular canals. Dietary measures such as salt restriction, are also important.

 

E V O L U T I O N   O F  S Y M P T O M S

An acute vestibular episode is generally, within a few weeks followed by central cerebral compensation. Compensation leads to a state in which the patient is asymptomatic. Due to neural damage, this state may reverse to a state of dizziness in times of physical or psychological stress, leaving the patient with an intermittent long-term balance disorder. Patients with chronic vestibular dysfunction generally have a past history of an acute vestibular episode.

 

D I A G N O S I S - H I S T O R Y  T A K I N G

The key to diagnosis is to spend enough time in history taking. Time at this stage in the consultation is time well spent. Onset and the circumstances surrounding onset of vertigo are important. Increasing age is related to a sharp rise in incidence of unsteadiness. There is an age-related degeneration of otoconia, vestibular epithelia and neurons and vascular insufficiency, together with a degeneration of vision and proprioception.

Any previous episodes are relevant. Sometimes patients describe more that one discrete sensation of dizziness. Was there any previous head injury? Any factors making the sensation worse, including change in position, are noted. Were there any premonitory warnings such as fullness in the ear, visual aura or skin rash around the auricle?

Symptoms such as deafness, pain aural discharge, tinnitus and facial weakness point to an otological cause. Other central nervous signs including visual disturbances, headaches, weakness in the limbs, dysphonia, dysphagia are relevant. Loss of consciousness is not a feature of vestibular disease.

 

Cardiac arrythmias (palpitations), hypertension, hypotension (including over-treatment of hypertensive patients), embolism from diseased heart valves and interference with the vertebrobasilar blood supply may all give dizziness. Metabolic causes of dizziness include diabetes, by means of hypoglycaemia and autonomic neuropathy.

Vitamin B deficiency neuropathy may be seen in alcoholics.

In patients with anxiety attacks, hyperventilation is often followed by lightheadedness.

 

P H Y S I C A L  E X A M I N A T I O N

 

The ears are examined to exclude active disease such as otitis media and cholesteatoma. Tuning fork tests and hearing assessment are important to evaluate conductive losses and also, unilateral sensorineural losses such as in Meniere’s disease. The rest of the ENT examination includes the neck (cervical problems may also be a cause of unsteadiness). The cranial nerves are assessed together with eye movements (nystagmus) and papillary reactions. Stance, gait and muscle coordination (test for cerebellar signs) are evaluated, together with a basic assessment of cardiovascular function and peripheral vibration sense.

 

INVESTIGATIONS

 

In the caloric test warm (44 C) or cold water (30 C) kept in two tanks is run into the patients’external auditory meatus for 40 seconds. Alternate ears are tested to ‘rest’ each ear, eg cold right, cold left, warm right, warm left. The patient should be positioned with the head flexed at 30o. Irrigating the ear canal causes convection currents in the lateral semicircular canal (that canal most superficial to the medial wall of the middle ear). Movement of endolymph causes cupular movement. The hair cells inserting into the cupula are stimulated setting up a VOR.

The beginning of the irrigation is taken as time zero and the duration in which nystagmus occurs is recorded till it subsides even during fixation at a fixed point on the ceiling.

The end-point is recorded when the nystagmus ceases. If nystagmus is enhanced in one way or another this is called directional preponderance. Should there be an absent response this is called a canal paresis and indicates loss of function of vestibular labyrinth, nerve or nuclei.

 

Imaging

Blood tests are to be guided by the history and physical examination. A complete blood count and blood glucose estimation are useful basic tests. Magnetic resonance imaging of the cerebello-pontine angle is the modality of choice especially if there is suspicion of a small lesion in the internal auditory canal.

 

Drug treatment

Vestibular sedatives are used for acute phase and then should be stopped as patient symptoms improve through central compensation.

The primary aid of vestibular rehabilitation is to make the patient as independent as possible. This consists of a proper diagnosis of peripheral vestibular disease and then the graded introduction of physical exercises designed to challenge the remaining vestibular system in order to attain the maximum mobility for that patient. Long-term use of vestibular sedatives makes the possibility of drug interactions and sedation increasingly likely.

Drugs that may cause dizziness include antihistamines, psychotropic drugs, antihypertensives, antimicrobials (eg aminoglycosides), analgesics, hormone replacement and chemotherapeutic agents.

 

 


 

 

REFERENCES

 

  1. Roydhouse N. Vertigo and its treatment. Drugs. 1974;7(3):297-309
  2. Davison J, Bond J, Dawson P et al. Patients with recurrent falls attending Accident & Emergency benefit from multifactorial intervention-a randomized controlled trial. Age Aging 2005 34(2); 162-8
  3. Yardley L, Burgneay J, Nazareth I, Luxon L Neuro-otological and psychiatric abnormalities in a community sample of people with dizziness: a blind, controlled investigation. J Neurol Neurosurg Psychiatry 1998 65(5); 679-84
  4. Sloane PD, Coeytaux RR, Beck RS et al Dizziness:state of the science. Ann Intern Med. 2001; 134 (pt 2); 823-32
  5. Baloh RW, Sloane PD, Honrubia V. Quantitative vestibular function testing in elderly patients with dizziness. Ear Nose Throat J 1989; 68 (12); 935-9
  6. Sekine K, Sato G, Takeda N. Incidence of vertigo and dizziness disorders at a University Hospital. Nippon Jibiinkoka Gakkai Kaiho.2005; 108 (9); 842-9
  7. LeopardiG, Chiarella G, Serafini G et al. Paroxysmal positional vertigo:short- and long-term clinical and methodological analyses of 794 patients. Acta Otorhinolaryngol Ital 2003; 23(3), 155-60
  8. Epley, J.M. The canalith repositioning procedure for treatment of benign paroxysmal positional vertigo. Otolaryngol- Head Neck Surg 1992; 107, 399-404
  9. Semont, A., Freyss, G., and Vitte, E. Curing the BPPV with a liberatory maneuver. 1988. Adv Otorhinolaryngol. 42; 290-293

 

 

 


 

 

FURTHER READING

 

BPPV: http://www.emedicine.com/ent.topic761.htm

Migraine and vertigo: http://www.emedicine.com/ent.topic727.htm

Vestibular rehabilitation : http://wwwemedicine.com/ent/topic666htm

 

Ó Mr. Adrian M Agius

Last modified on Thursday, 21 February 2019 10:18