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Update on the Bedside Evaluation of the Dizzy Patient: the Angular and Transalational Vestibuloocular Reflex

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Update on the Bedside Evaluation of the Dizzy Patient: the Angular and Transalational Vestibuloocular Reflex 대한평형의학회지 제 4 권 1 호 2005 ; 145-158 Update on the Bedside Evaluation of the Dizzy Patient: the Angular and Transalational Vestibuloocular Reflex David Zee The Johns Hopkins University, USA Basic Physiological Principles • Two types of acceleration sensors: angular (semicircular canals) and linear (otoliths) • Two reflexes: vestibulo-ocular reflex (VOR) and vestibulo-spinal reflex (VSR) • Functions: Assure clear vision during head motion (rotation and translation) and maintain upright posture during standing and walking 145 Update on the Bedside Evaluation of the Dizzy Patient: the Angular and Transalational Vestibuloocular Reflex Central labyrinthine projections Innervation and Blood Supply of the Labyrinth: Clinical points SCC – rostral vestibular complex • Anterior vestibular artery is an end artery (hence most susceptible to ischemia). Thus posterior circulation hypoperfusion with isolated vertigo is a possibility albeit unusual to recur over the long term without other signs or symptoms. • Cochlear branch of the common cochlear -- posterior vestibular artery supplies the basal turn of the cochlea (high frequencies). Hence hearing loss in association with ischemic (and inflammatory) processes on the vestibular nerve is usually high OTOLITH – caudal frequency while with Ménière's disease vestibular complex (endolymphatic hydrops) the hearing loss with vertigo is usually low frequency. SCC / Otolith VESTIBULOCEREBELLUM SCC Organization: a guide to nystagmus Central projections from the labyrinth Arrows indicate direction of • SCC projections are primarily to the rostral slow phase with stimulation portions of the vestibular complex. • Otolith projections are primarily to the caudal portions of the vestibular complex. Beware infarct in lateral medulla (Wallenberg’s syndrome) when symptoms and signs are isolated otolith (tilt, vertical diplopia due to skew (vertical misalignment of eyes). • SCC and otoliths also project directly to the cerebellum. Beware of cerebellar hemorrhage and Central Patterns infarct in elderly presenting as ‘labyrinthitis’, especially if they CANNOT walk, even with assistance. Peripheral Pattern Why do vestibular patients complain so much in Visual-Vestibular Interaction: supermarkets, while driving, watching action movies? convergence of labyrinthine and visual inputs within the vestibular nuclei There is a strong convergence between vestibular and visual signals in the brainstem (vestibular nuclei) and cerebrum (vestibular cortex). Rotation in the In pathological circumstances, the visual and dark vestibular signals become incongruent, leading to abnormal sensations of motion and tilt, and discomfort, anxiety and phobias. Pure visual (optokinetic) input 146 David Zee Psychiatric disease and vertigo A physiological based exam • Disabling psychological effects of vestibular disease. – Phobic behavior. • Static disturbances due to a tone imbalance – Anxiety and panic attacks. with head still. – Depression and withdrawal. • Psychiatric disease presenting with vestibular • Dynamic disturbances due to abnormal responses symptoms during motion of the head – Somatization and psychosomatic disorders. – Obsessive compulsive behavior. – Panic attacks. – Depression. Evaluation and treatment of psychiatric symptoms in vestibular patients should proceed in parallel with the ‘organic’ evaluation and treatment Bedside Examination of the SCC – static disturbances LOCALIZATION OF NYSTAGMUS – Peripheral lesions – Nystagmus is increased or brought out by removal of fixation (Romberg sign of VOR) – Mixed horizontal-torsional nystagmus is characteristic for complete loss of function on one side – Central lesions – Fixation has little effect on nystagmus – Pure vertical or pure torsional nystagmus 147 Cerebellar Control of Eye Movements Dynamic Visual Acuity (DVA) Normal subjects lose only 1 line of acuity with head shaking. Patients with no vestibular function lose about 5 lines with horizontal or vertical rotation but not with rotation in ‘roll’ (ear to shoulder) since the image is still on the fovea. Patients who lose DVA in ‘roll’ are malingering! Head-thrust sign in bilateral labyrinthine Technique to elicit thrusts (rotational VOR) loss and heaves (translational VOR) Catch-up saccades during brief, high- acceleration, head rotation (bilateral loss) Remember: Patients who lose vestibular function bilaterally do NOT have vertigo since there is no tone imbalance or nystagmus. E.g., ototoxicity of antibiotics Vestibular responses on the ‘head sled’ Quantification of t-VOR: ‘Head sled’ Normal subject Cerebellar patient 148 David Zee Pursuit -- Cerebellar patient Head-shaking induced nystagmus • Peripheral pattern: slow phase toward affected ear after horizontal head shaking • Central pattern: vertical nystagmus (usually DB) after horizontal head shaking (cross coupling) • Note that in Ménières disease the initial slow phase may be toward the intact ear. Can not use the direction of nystagmus to decide the affected ear in Ménières disease. Must use audiogram and hearing. 149 Cerebellar Control of Eye Movements Mechanisms for hyperventilation-induced Congenital Epidermoids nystagmus • Usually appear in adolescence • Improved conduction on demyelinated fibers • Males > females (alkalosis, calcium). • Change in intracranial pressure mediated • Hemifacial spasms may precede frank through a fistula. facial palsy • Seizures. • Ischemia (decreased blood flow). Recovery nystagmus • After a unilateral peripheral loss of vestibular function there is a central rebalancing to eliminate the spontaneous nystagmus. • If peripheral function suddenly “recovers” (e.g., by improved conduction on demyelinated nerves because of pH changes due to hyperventilation), a new imbalance is created causing a recovery nystagmus with slow phases directed away from the affected ear. Fistula due to dehiscence of the roof of the superior SCC Intact side Abnormal side Lloyd minor CT temporal bone 0.5mm slices with 3D reconstruction Beldon, Radiology 2003 150 David Zee Audiograms in superior canal dehiscence Vestibular-evoked myogenic potentials (VEMPS) Air-bone gap • Short-latency, relaxation potentials measured from tonically-active sterno- cleido-mastoid muscle that relax with Case1 Lowered threshold ipsilateral loud clicks. for bone-conducted • Originate from the sacculus (inferior hearing division of vestibular nerve) • 10 Hz, 0.1ms, 60-103 dB Case2 151 Cerebellar Control of Eye Movements Syndrome of dehiscence of the roof of the superior canal • Vertigo, oscillopsia, and/or dysequilibrium related to noise, altered middle ear pressure, exercise and/or altered intracranial pressure (e.g., Valsalva maneuvers, jugular vein compression). • Changes in symptoms with head position; chronic dysequilibrium. • Auditory findings – Gaze-evoked and pulsatile tinnitus – Hyperacusis – lowered thresholds for bone conduction with air-bone but with normal tympanogram – ‘Malleolus sign’ (hears vibration at ankle!) – Lowered threshold for click-induced EMG of sternocleidomastoid (VEMPs) Syndrome of dehiscence of the roof of the superior canal Migraine and • Induced vertical-torsional eye movements (with the vestibular sound or valsava maneuvers) that can be system explained by activation of the superior canal. • Temporal bone CT scans identify dehiscence of bone overlying the affected superior semicircular canal. • Beware some normals without symptoms have thin bone. Von Brevern, Brain, 2004; Neurology 2004 • Beware false positives (especially with > 0.5mm Furman, JNNP,2005 sections). Neuhauser, Cephalgia, 2004 • Symptoms relieved by plugging of the superior canal (if necessary). Crevitz, Clinical Neurology Neurosurgery, 2005 Brantberg, Acta Otolaryngologica, 2005 Some ‘facts’ about vestibular migraine Some ‘facts’ about vestibular migraine • In a “dizziness clinic” 38% of patients were • The mean onset of vertigo in migraine is about 40 diagnosed with migraine (24% in an orthopedics clinic); 7%, with migrainous vertigo, and in a yrs of age, and headaches precede vertigo by “migraine clinic”, 9% diagnosed with migrainous almost 10 years. Women much more likely to be vertigo. (Neuhauser). diagnosed with vertigo and migraine. • Other studies suggest that more than 50% of • Duration of symptoms is usually minutes to a day migraineurs have vestibular symptoms (including but ‘low-level’ symptoms may last days to weeks – dizziness)! imbalance and extreme motion sensitivity • In patients with dizziness and migraine, • Patient may have hearing symptoms; muffled abnormalities on vestibular lab testing are common, sounds, ear pressure or pain, tinnitus. but often nonspecific. – up to 25% of migraineurs with dizziness have been • Patients overall often have chronic motion reported to have a reduced caloric response. (CAUTION sensitivity. (Syndrome of mal de debarquement). ADVISED HERE). • Migraine headaches are often an infrequent or – Interictal, central eye movement abnormalities (e.g., gaze-evoked nystagmus, impaired pursuit) have been long-forgotten symptom in vestibular migraine. reported in as many as 65% of patients with migraine • Migraine headaches may occur independently of and vestibular symptoms. (CAUTION ADVISED HERE but note reports of subclinical cerebellar dysfunction vestibular symptoms and vice versa. Often they (limb dysmetria) in migraine.) never occur together. 152 David Zee Some ‘facts’ about vestibular migraine Differential diagnosis of vestibular migraine • Vestibular neuritis, neuronitis, labyrnthitis, • Family history is usually positive and neurolabyrinthits
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