<p>The positional characteristics of vertigo are often attributed to a peripheral origin, which may lead to diagnostic errors. Downbeat nystagmus (DBN), a marker of cerebellar dysfunction, can be imperceptible in primary gaze and only become evident after positional manoeuvres, which tend to enhance an otherwise subtle nystagmus. We present two elderly patients with progressive cerebellar ataxia and DBN that was barely present in primary gaze but clearly enhanced in the supine position. Both exhibited additional central oculomotor signs and bilateral vestibulopathy, without significant structural lesions on neuroimaging. Genetic testing confirmed SCA27B in one case and CANVAS syndrome in the other. These findings highlight the value of positional manoeuvres not only in diagnosing BPPV but also in unmasking central DBN. Recognizing positional enhancement as part of DBN’s clinical spectrum prevents misclassification as true positional nystagmus and increases the sensitivity of bedside examination, facilitating earlier recognition of degenerative cerebellar syndromes. In conclusion, positional manoeuvres are indispensable tools in neurology practice, capable of revealing subtle DBN and contributing to the timely diagnosis of progressive cerebellar disorders.</p>

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Enhancing Cerebellar Findings with Positional Manoeuvres

  • Carmen María Sánchez García,
  • Hüseyin Nezih Özdemir,
  • Diego Kaski

摘要

The positional characteristics of vertigo are often attributed to a peripheral origin, which may lead to diagnostic errors. Downbeat nystagmus (DBN), a marker of cerebellar dysfunction, can be imperceptible in primary gaze and only become evident after positional manoeuvres, which tend to enhance an otherwise subtle nystagmus. We present two elderly patients with progressive cerebellar ataxia and DBN that was barely present in primary gaze but clearly enhanced in the supine position. Both exhibited additional central oculomotor signs and bilateral vestibulopathy, without significant structural lesions on neuroimaging. Genetic testing confirmed SCA27B in one case and CANVAS syndrome in the other. These findings highlight the value of positional manoeuvres not only in diagnosing BPPV but also in unmasking central DBN. Recognizing positional enhancement as part of DBN’s clinical spectrum prevents misclassification as true positional nystagmus and increases the sensitivity of bedside examination, facilitating earlier recognition of degenerative cerebellar syndromes. In conclusion, positional manoeuvres are indispensable tools in neurology practice, capable of revealing subtle DBN and contributing to the timely diagnosis of progressive cerebellar disorders.