How to differentiate problematic dizziness
A wide range of problems may present with dizziness or vertigo ENT specialist
Dr Rudrapathy Palaniappan outlines the differentiating tests and management plans
Dizziness is a common symptom and is responsible for considerable handicap and psychological morbidity. When it comes to the diagnosis and management of a dizzy patient, a holistic approach is paramount. Dizziness is a non-specific symptom and does not instantly point to any specific organ systems. Balance function is an integrated phenomenon and involves the interplay of at least three different sensory inputs.
Disequilibrium may result from disturbance in a number of structures, including visual, proprioceptive, vestibular, cardiovascular and central nervous system. Peripheral vestibulopathy is the cause of dizziness in a large proportion of patients and responds well to appropriate vestibular rehabilitation exercises.
Making a diagnosis
In the majority of patients a carefully obtained thorough history combined with targeted physical examination should yield a successful diagnosis.
The term dizziness is commonly used to cover four broad categories of balance dysfunction vertigo, disequilibrium,
near-syncope and non-specific light-headedness. Vertigo is defined as an illusion or hallucination of movement and is typically thought to arise from an abnormality involving the peripheral or central vestibular pathways.
A clear-cut distinction needs to be made between vertigo and non-specific light-headedness, dizziness or faintness, which may be caused by a variety of general medical conditions. As a general rule, disorders affecting the peripheral vestibular system often cause associated hearing impairment. But conditions such as benign paroxysmal positional vertigo (BPPV), vestibular neuronitis and familial vestibulopathy selectively affect the peripheral vestibular system without any hearing loss.
Historical features that help distinguish peripheral from central vertigo include:
lpresence in the peripheral vertigo and absence in central vertigo of hearing loss
lnausea and vomiting tends to be severe in peripheral rather than in central vertigo
lassociated neurological symptoms are rare in peripheral vestibular disorders as opposed to central vestibular dysfunction
lcompensation is rapid with peripheral vestibular failure and is slow or incomplete in central vestibular disturbance.
Because not all dizziness is vertigo, even though patients may describe vertigo as dizziness, it is useful to get the patient to describe the exact sensation and associated symptoms such as nausea, vomiting or headache.
Vertigo associated with hearing loss
Vertigo associated with hearing loss may be a manifestation of Meniere's disease, temporal bone fracture, otitic barotrauma, perilymph fistula, vestibular schwannoma, labyrinthitis, otosyphillis, ototoxic drugs and autoimmune inner ear disease.
Benign paroxysmal positional vertigo
BPPV is one of the most common causes of dizziness and is thought to arise from the presence of abnormal dense particles (most likely otoconial debris) in the posterior semi-circular canal.
BPPV is characterised by severe, brief paroxysms of rotational vertigo provoked by positional changes. Hallpike's positional test provokes dizziness and a typical geotropic nystagmus is diagnostic of this condition. If reliance is made only on the history for diagnosis without Hallpike's test, approximately a quarter of patients with BPPV may be missed. Canalith repositioning procedure is effective in most cases.
Vestibular neuronitis (VN) is another common cause for peripheral vestibular vertigo. Sudden onset of severe vertigo with nausea, vomiting and absence of auditory symptoms typify VN.
Characterised by endolymphatic hydrops, Meniere's disease presents itself with spontaneous recurrent episodic vertigo, fluctuating sensorineural hearing loss, tinnitus and a feeling of pressure in the ear.
It is a diagnosis of exclusion, since other pathologies such as acoustic neuroma and otosyphillis may present as endolymphatic hydrops. It is a unilateral disorder in most cases, but may rarely affect both ears. Most patients can be managed conservatively by medical treatment, but a small proportion may require surgical intervention.
The term cervical vertigo (CV) should be restricted to cases where the underlying mechanism is alleged to be one of defective neck proprioception. Vertigo associated with neck movements could result from disorders of vestibular, visual, vascular, neurovascular, or cervico-proprioceptive mechanisms.
The lack of specific diagnostic tests for CV makes the diagnosis controversial. There are claims that dizziness of cervical origin might result from cervical tone imbalance, secondary to either loss or inadequate stimulation of neck receptors. But such a tone imbalance has not been demonstrated in whiplash injuries or cervical pain syndromes.
If true cervical vertigo exists the treatment is similar to that of the underlying neck condition.
Bilateral vestibular failure
Bilateral vestibular failure (BVF) may present with recurrent episodes of vertigo associated with unsteadiness in the dark and oscillopsia (oscillating vision) on head movement. Ototoxic drugs such as gentamycin commonly cause BVF, which may frequently be associated with some degree of high frequency sensorineural hearing loss.
Management of patients with bilateral vestibular loss is difficult and involves maximising and optimising visual and proprioceptive inputs. Counselling should include safety considerations such as night-lights at home, assistive devices and warning about the risk of drowning with diving.
Migraine and vertebrobasilar transient ischaemia are the common central causes of recurrent spontaneous vertigo. Brain stem and cerebellar lesions can cause a persistent positional vertigo with downbeat, upbeat or torsional nystagmus.
Symptomatic improvement in peripheral vestibular lesion is not due to restoration of normal labyrinthine function but is the result of compensation. Compensation is a central process, therefore peripheral lesions tend to compensate more readily than brain stem or cerebellar causes. Approximately 80 per cent of patients respond favourably to vestibular rehabilitation exercises.
Long-term use of vestibular sedatives may delay compensation, although they are useful in the acute management of vertigo. Other causes include inappropriate exercise strategy, poor vision, concomitant untreated cardiac/neurological/haematological disorders and psychological factors such as avoidance behaviour and anxiety.
Treatment and management
Treatment begins with counselling, which involves explaining the balance mechanism to the patient within a framework of vestibular physiology. Specific vestibular rehabilitation exercises such as Cawthorne-Cooksey (see box) or Herdman's eye exercises would help promote central compensation. Particle repositioning manoeuvre is effective in benign paroxysmal positional vertigo as are other vestibular exercises.
Central positional vertigo and bilateral peripheral vestibular dysfunction are difficult management entities.
Reassurance is an essential aspect of management. Beliefs, emotions, interactions within the limbic system and the individual's psychological profile all affect balance function and may lead to depression, anxiety or stress. Psychological interventions, cognitive behaviour therapy and antidepressants may be required in some individuals.
Hyperventilation may be an aggravating factor. Relaxation and breathing exercises are useful in some cases.
Elimination of caffeine and dietary regulation may be helpful in Meniere's disease and migraine-related vestibulopathy.
· Pure tone audiogram
· Full blood count
· Magnetic resonance imaging
· Stapedial reflexes
· Urea and electrolytes
· X-ray of cervical spine
· Auditory brain stem responses
· Fasting blood sugar
· Magnetic resonance angiography
· Serum lipids
· Transcranial doppler ultrasound
· Posturography (Equitest)
· Thyroid function tests
· Caloric test
· Serology for syphilis
· Autoimmune profile
In bed or sitting
· Eye movements (slow initially, then quick): up and down; from side to side; focusing on a finger moving from three feet to a foot from the face
· Head movements (initially slow, then quick, and later with the eyes closed): bending forward; turning from side to side
· Eye movements and head movements as above
· Shoulder shrugging and circling
· Bending forward and picking up objects from the ground
· Eye, head and shoulder movements as above
· Changing from sitting to standing position with eyes open and shut
· Throwing a small ball from hand to hand (above eye level)
· Throwing a ball from hand to hand under knee
· Changing from sitting to standing and turning around in between
1 Bath AP et al. Experience from a multidisciplinary 'dizzy' clinic. Am J Otol 2000;21:92-7
2 Brandt T, Bronstein AM. Cervical vertigo.
J Neuro Neurosurg Psychiatry 2001;71:8-12
3 Epley JM. Particle repositioning for benign paroxysmal positional vertigo. Otolaryngol.
Clin. North. Am. 1996;29:323-31
4 Luxon LM. The medical management of vertigo.
J Otol Laryngol 1997;111: 1114-21
5 Palaniappan R. Balance disorders in adults: an overview. Hospital Medicine 2002;63:278-81
6 Royal College of General Practitioners and
Office of Population Census and Surveys. Morbidity statistics from General Practice. London: HMSO, 1986
7 Assessment and treatment of complete vestibular loss. In: Vestibular rehabilitation. Herdman (ed.), 2nd edition. Philadelphia, FA Davies. 2000