Vertigo

Southern Neurology

Dizziness – is it vertigo ?

Is the dizziness is vertiginous in nature, or more suggestive of near-syncope or non-vestibular dizziness

Is the dizziness is affected by movements of the head, if so it suggests a peripheral vertigo

         a patient with peripheral acute vertigo often prefers to sit upright and not lie down, or prefers to lie still with the unaffected ear undermost; and the patient also prefers to avoid any sudden head movements

         a patient with central vertigo often has a lesser degree of dizziness, which is less affected by head movements and not specifically related to a particular head position

Dizziness and head movement

Vertigo lasting seconds, which is only precipitated by sudden movements of the head (looking up, suddenly twisting the head, suddenly getting up from a supine position or when suddenly rolling over in bed) suggests benign positional vertigo

         a patient with benign positional vertigo may be able to identify a particular movement or position of the head that precipitates vertigo, which usually occurs after a latent period of 10 - 20 seconds

         patients with BPV may complain of non-specific nausea, dysequilibrium and dizziness between attacks

Dizziness – duration assists differential diagnosis

The duration of the vertigo provides useful information          vertigo lasting seconds suggests benign

paroxysmal positional vertigo          vertigo lasting minutes suggests transient

cerebrovascular ischaemia (posterior circulation TIA)          vertigo lasting hours suggests Meniere's syndrome          vertigo lasting hours-days suggests vestibular

neuronitis or posterior circulation strokes

Dizziness and otological symptoms

Deafness and/or tinnitus suggests peripheral vertigo          Many patients with vestibular neuronitis have a history

of a recent viral illness in the past few weeks. Otological symptoms in a patient with acute vestibular neuronitis suggests acute (serous) labyrinthitis

         Recent severe earache +/- ear discharge +/- fever suggests a middle ear infection and a possible acute (purulent) labyrinthitis

         Recent head trauma, sudden coughing/sneezing + sudden 'pop' in the ear, or recent scuba diving suggests a possible peri-lymphatic fistula (vertiginous symptoms may also be exacerbated by valsalva-type maneuvers or a loud noise)

Benign positional vertigo theory 1

Cupulolithiasis theory In 1962, Dr Harold Schuknecht proposed the cupulolithiasis

(heavy cupula) theory. Via photomicrographs, he discovered basophilic particles or densities that were adherent to the cupula. He postulated that the PSC was rendered sensitive to gravity by these abnormal dense particles attached to, or impinging on, the cupula. This is analogous to the situation of a heavy object attached to the top of a pole. The extra weight makes the pole unstable and thus harder to keep in the neutral position. This produces persistent nystagmus and also explains the dizziness when a patient tilts the head backward.

Benign positional vertigo theory 2

Canalithiasis theory In 1980 Epley published his canalithiasis theory. He believed

that the symptoms of BPPV were more consistent with free-moving densities (canaliths) in the PSC rather than fixed densities attached to the cupula. While the head is upright, the particles sit in the PSC at the most gravity-dependent position. When the head is tilted back supine, the particles are rotated up to about 90 degrees along the arc of the PSC. After a momentary (inertial) lag, gravity pulls the particles down the arc. This causes the endolymph to flow away from the ampulla and causes the cupula to be deflected. The cupular deflection produces nystagmus.

Benign positional vertigo -epidemiology

In one U.S. study, the age- and sex-adjusted incidence was 64 per 100,000. Incidence in general population is higher in persons older than 40 years. In a recent study of a group of elderly patients, the incidence was found to be approximately 8%. BPPV may represent a health hazard to the elderly. Estimates suggest that approximately 20% of all falls that result in hospitalization for serious injuries in the elderly are due to vertigo of end-organ origin (most often related to BPPV).

Average age of onset 51 years. M=F, although some studies show a slight predilection for women.

It is rarely seen in persons younger than 35 years without a history of antecedent head trauma.

Causes of BPV –in a study of 240 patients

Idiopathic – 118 cases Posttraumatic – 43 cases Viral neurolabyrinthitis – 37 cases Other – VBI 11 cases

Meniere’s disease 5 cases

Post-surgical 10 cases (including 5 ear surgery)

Ototoxicity 4 cases

Nystagmus

  Appearance Latency Duration Fatigability Localisation

Central  Pure vertical, usually downbeat

Unusual Persistent Unusual Brainstem or cerebellum

Peripheral Torsional upbeat or horizontal geotropic

Usual Brief Usual Posterior or horizontal semi-

circular canal

Epley manouevre

Exercise therapy at home

Horizontal and anterior canal BPV

Vast majority are due to posterior semicircular involvement. Anterior canal BPV – torsional downbeating not upbeating

nystagmus during Hallpike test induced when the abnormal anterior canal (which lies at right angles to posterior) is uppermost. Repositioning manouevre starts with abnormal ear uppermost – moving across to opposite head hanging position.

Horizontal canal BPV – rare, paroxysmal horizontal direction changing nystagmus –beats towards ground when head turned to side while patient lies supine. Nystagmus lasts 1 minute, minimal latency and no fatiguability. Occurs with head to either side but stronger on one side. Treatment is a 360 degree log roll in 90 degree steps to normal side prone, to abnormal side and then supine.

Vestibular neuronitis

Acute, prolonged vertigo of peripheral origin is commonly called vestibular neuritis, although other terms such as "vestibular neuronitis," "labyrinthitis," "neurolabyrinthitis," and "unilateral vestibulopathy of unknown cause" have also been used.

The vertigo typically develops over a period of hours, is severe for a few days, and then subsides over the course of a few weeks.

Some patients can have residual nonspecific dizziness and imbalance that lasts for months or longer. with known viral disorders of the inner ear, such as measles and mumps.

Vestibular neuronitis -pathophysiology

The condition is thought to result from a selective inflammation of the vestibular nerve, presumably of viral origin.

The facts that the disorder often has a viral prodrome, that it occurs in epidemics, that it may affect several members of the same family, and that it occurs more commonly in spring and early summer all support a viral cause.

Postmortem studies have found atrophy of the vestibular nerve and the vestibular sensory epithelium that is similar to the pathological findings.

Clinical features of vestibular neuronitis

Mean age 41.5 years, 55% are males Sudden vertigo, often overnight; 66% noted on

awakening. Severity peaks within first day. Direction-fixed horizontal nystagmus with fast phase

towards healthy ear. Intensity of nystagmus increases with gaze toward healthy ear and decreases with gaze towards affected ear.

Frenzel glasses, which prevent visual fixation, may be needed to observe spontaneous nystagmus.

Head-impulse test is positive

Frenzel glasses

Head impulse (or thrust) test

A simple bedside test of the horizontal vestibulo-ocular reflex performed by grasping the patient's head and applying a brief, small-amplitude, high-acceleration head turn, first to one side and then to the other.

To start, the eyes should be about 10 degrees away from the primary position in the orbit so that after a 10-degree head turn, the eyes will be near the primary position.

The patient fixates on the examiner's nose and the examiner watches for corrective rapid eye movements (saccades), which are a sign of decreased vestibular response (i.e., the eyes move with the head rather than staying fixed on the nose).

In ‘peripheral’ lesions (labyrinth or the 8th nerve including the root's entry zone in the brain stem) a"catch-up" saccades occur after head thrusts in one direction but not the other.

Vestibular neuronitis – time course

Disabling severe vertigo lasts less than 1 week in 70%; and less than 2 weeks in 96%.

However, caloric testing shows partial canal paresis in 30% and absent responses in 10-20% at 1 year.

In one long term clinical follow-up study, minor symptoms (transient vertigo with rapid head movements or slight unsteadiness) persisted for 3 months in 60%, 1 year in 50% and more than 5 years in 25%.

Meniere’s disease

15-46/100,000 population per year affected in USA.

By definition – idiopathic endolymphatic hydrops.

2 phases – early (almost always unilateral and symptoms episodic) and late (symptoms present more or less all the time with episodes of exacerbation consisting of an increased severity of symptoms).

Clinical features of Meniere’s disease

Vertigo – well defined episodes, 20 min – 24 h duration, frequent nausea/vomiting, vestibular nystagmus may be present.

Deafness – sensorineural, fluctuating, progressive. During attacks hearing loss may be sudden, lasts minutes to hours to days to weeks. May remain as permanent deficit.

Tinnitus – variable, episodic, begins slowly, may reach crescendo over minutes to hours, continues for hours to days to weeks.

Aural pressure – most variable of symptoms.

Treatment of Meniere’s disease

Meniere’s crisis has been reported after high sodium meal. This has led to treatments recommending moderate sodium restriction (1-2 g sodium/day). Often strict sodium restriction (<1g/day) required.

Diuretics – mixed results in double blind studies. A retrospective study showed beneficial hearing effects of diamox and chlorthalidone in short-term (2-6 weeks) but not long term (5 years).

Histamine (vasodilates labyrinth vasculature)– short-term benefits only; vestibular suppressants – no long term advantage.

Surgery – destructive (need to warn patient of risks if contralateral ear becomes affected) and non-destructive (eg endolymphatic sac decompression) procedures

ENG and calorics

Caloric testing – cold and warm water irrigation

Other causes of peripheral vertigo

Migraine-associated vertigo Post-traumatic – “whiplash” injury is frequently

associated with vertigo – often difficult to explain particularly if neuro-imaging is negative for high cervical nerve damage.

Perilymphatic fistula – penetrating ear trauma, temporal bone or head trauma, prior stapedectomy and barotrauma. Patients experience stepwise progressive sensori-neural hearing loss with episodes triggered by exertion or Valsalva and episodic and/or positional vertigo triggered by exertion or Valsalva.

Causes of central vertigo

Infarcts - the absence of associated neurological symptoms does not exclude central vertigo because as many as ~ 25% of middle-aged/elderly patients with risk factors for stroke, who present to the ED with isolated severe vertigo +  postural instability may have an inferior cerebellar infarction

Cerebellopontine angle tumors

Multiple sclerosis

Vertebral artery or PICA infarct causing lateral medullary syndrome

Vertigo, nystagmus Gait and limb ataxia Dysphagia, decreased gag Ipsilateral facial hemianaesthesia Ipsilateral Horner’s syndrome Contralateral arm/trunk/leg pain and

temperature (spinothalamic) loss

Lateral medullary infarction

Multiple sclerosis

Visual evoked potentials

Vertigo in multiple sclerosis

At least 5% of patients with MS report vertigo as an initial symptom.

Vertigo may be rotatory with a positional component in some patients.

Diplopia, facial paraesthesia and weakness may co-exist.

Eye signs in MS patients with vertigo can include nystagmus, internuclear ophthalmoplegia and abnormal saccades (eg dysmetria, slow saccades), impaired pursuit and impaired convergence.

Cerebello-pontine angle tumours

Other central causes