Head-shaking nystagmus in lateral medullary infarction - Patterns and possible mechanisms

Pusan National University, Tsau-liang-hai, Busan, South Korea
Neurology (Impact Factor: 8.29). 05/2007; 68(17):1337-44. DOI: 10.1212/01.wnl.0000260224.60943.c2
Source: PubMed


Horizontal head shaking at 2 to 3 Hz can induce nystagmus in patients with central as well as in patients with peripheral vestibulopathy. However, the characteristics and diagnostic value of this post-head-shaking nystagmus (HSN) have not been studied systematically in central vestibulopathy, and little is known of the mechanisms involved.
We analyzed spontaneous and HSN and the effects of baclofen, a GABA(B) agonist, in 16 patients with acute lateral medullary infarction.
These patients showed several characteristics of HSN unlike those observed in peripheral vestibulopathy. HSN was observed in 14 of 16 patients (87.5%), and in all cases, the horizontal component beats toward the lesion side, i.e., was ipsilesional. Even in the eight patients with contralesional spontaneous horizontal nystagmus, the HSN was opposite to the spontaneous nystagmus. Three patients showed unusually strong HSN with a maximum slow-phase velocity greater than 60 degrees/second. Visual fixation markedly suppressed HSN and baclofen reduced HSN. In most of the patients, MRI showed infarctions in the caudal or middle portion of the medulla and spared the rostral portion.
We propose that head-shaking nystagmus in lateral medullary infarction is due to unilaterally impaired nodulouvular inhibition of the velocity storage. This proposal is consistent with the results of neuroanatomic studies that demonstrate that Purkinje cells controlling velocity storage in the nodulus and ventral uvula project to the caudal or middle portion of the vestibular nuclei, whereas those subserving visual-vestibular interactions in the flocculus project to the more rostral portion.

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    • "Head-shaking nystagmus (HSN) can be assessed using either a passive (by the examiner) or active (by the patient) head-shaking maneuver. The patient's head is pitched forward by approximately 20° to bring the horizontal semicircular canals (HCs) into the plane of stimulation, and then the head is shaken horizontally in a sinusoidal fashion at a rate of about 2-3 Hz with an amplitude of 20° for 15 seconds.26 In unilateral peripheral vestibulopathy, the typical pattern of HSN initially consists of contralesional nystagmus that decays over 20 seconds and then goes through a weak reversal.27 "
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    ABSTRACT: In recent decades there has been marked progress in the imaging and laboratory evaluation of dizzy patients. However, detailed history taking and comprehensive bedside neurotological evaluation remain crucial for a diagnosis of dizziness. Bedside neurotological evaluation should include examinations for ocular alignment, spontaneous and gaze-evoked nystagmus, the vestibulo-ocular reflex, saccades, smooth pursuit, and balance. In patients with acute spontaneous vertigo, negative head impulse test, direction-changing nystagmus, and skew deviation mostly indicate central vestibular disorders. In contrast, patients with unilateral peripheral deafferentation invariably have a positive head impulse test and mixed horizontal-torsional nystagmus beating away from the lesion side. Since suppression by visual fixation is the rule in peripheral nystagmus and is frequent even in central nystagmus, removal of visual fixation using Frenzel glasses is required for the proper evaluation of central as well as peripheral nystagmus. Head-shaking, cranial vibration, hyperventilation, pressure to the external auditory canal, and loud sounds may disclose underlying vestibular dysfunction by inducing nystagmus or modulating the spontaneous nystagmus. In patients with positional vertigo, the diagnosis can be made by determining patterns of the nystagmus induced during various positional maneuvers that include straight head hanging, the Dix-Hallpike maneuver, supine head roll, and head turning and bending while sitting. Abnormal smooth pursuit and saccades, and severe imbalance also indicate central pathologies. Physicians should be familiar with bedside neurotological examinations and be aware of the clinical implications of the findings when evaluating dizzy patients.
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    ABSTRACT: To determine chronological characteristics of vestibular recovery after vestibular neuritis (VN) by using various clinical parameters. Prospective clinical study. Twenty of 22 consecutive patients with acute VN underwent serial follow-ups of static (spontaneous nystagmus, subjective visual vertical, and ocular torsion) and dynamic (head-shaking nystagmus [HSN], vibration-induced nystagmus [VIN], head thrust test, and caloric test) vestibular imbalances for 1 year after symptom onset. Static vestibular imbalances improved more rapidly than dynamic imbalances. Among the dynamic imbalances, a trend of higher recovery rate was found in head thrust sign, HSN, and VIN than in caloric asymmetry. HSN tended to be more sensitive in detecting vestibular asymmetry than VIN and head thrust sign. Some patients showed direction reversal of HSN (n = 5, 25.0%) or VIN (n = 5, 25.0%) during follow-up. Direction of VIN changed according to the stimulation sites in four (20.0%) patients. In view of more rapid resolution of static vestibular imbalance after VN, evaluation of the dynamic vestibular imbalances may provide more useful information for underlying vestibulopathy, especially in the compensated phase. The different temporal profiles ofdynamic vestibular recovery may reflect different chronological characteristics of vestibular compensation according to stimulus frequency. Direction reversal of HSN and VIN during follow-up suggests that lateralization of VNbased on the direction of these nystagmus should be considered in the context of disease phase.
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