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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
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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 particularmovement 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
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 Nystagmus
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 originis commonly called vestibular neuritis, although other termssuch as "vestibular neuronitis," "labyrinthitis," "neurolabyrinthitis,"and "unilateral vestibulopathy of unknown cause" have also beenused. • The vertigo typically develops over a period of hours,is severe for a few days, and then subsides over the courseof a few weeks. • Some patients can have residual nonspecificdizziness and imbalance that lasts for months or longer. with known viral disordersof the inner ear, such as measles and mumps.
Vestibular neuronitis -pathophysiology • The conditionis thought to result from a selective inflammation of the vestibularnerve, presumably of viral origin. • The facts that the disorderoften has a viral prodrome, that it occurs in epidemics, thatit may affect several members of the same family, and that itoccurs more commonly in spring and early summer all supporta viral cause. • Postmortem studies have found atrophy of thevestibular nerve and the vestibular sensory epithelium thatis 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
Head impulse (or thrust) test • A simple bedside test of the horizontalvestibulo-ocular reflex performed by grasping the patient'shead and applying a brief, small-amplitude, high-accelerationhead turn, first to one side and then to the other. • To start,the eyes should be about 10 degrees away from the primary positionin the orbit so that after a 10-degree head turn, the eyes willbe near the primary position. • The patient fixates on the examiner'snose 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 fixedon the nose). • In ‘peripheral’ lesions (labyrinth or the 8th nerve including theroot's entry zone in the brain stem) a"catch-up" saccades occur after head thrustsin 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
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
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.
