Isolated Positional Downbeat Nystagmus: Central or Peripheral Positional Nystagmus? .
- Author:
Sun Young OH
- Publication Type:Original Article
- Keywords:
Nystagmus;
Positional vertigo;
Vestibulo-ocular reflex
- MeSH:
Cerebellar Ataxia;
Deception;
Dizziness;
Gait;
Head;
Head Impulse Test;
Healthy Volunteers;
Hearing;
Humans;
Neuroimaging;
Neurologic Manifestations;
Nystagmus, Physiologic*;
Paresis;
Pursuit, Smooth;
Reflex, Vestibulo-Ocular;
Saccades;
Vertigo
- From:Journal of the Korean Balance Society
2006;5(2):235-241
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OJBECTIVES: Nystagmus produced by static placement of the head in different orientations is termed positional nystagmus and in most instances the cause is a peripheral vestibular disorder, as in benign paroxysmal positioning vertigo (BPPV). However, the physiologic basis of the isolated positional downbeat nystagmus has not been fully understood. The goal was to find a possible pathomechanism of dizzy patients who showed isolated positional downbeat nystagmus (pDBN). MATERIALS AND METHOD: Twelve consecutive patients with isolated positional DBN and 50 normal volunteers underwent evaluation of spontaneous, head-shaking and positional nystagmus, smooth pursuit, saccades, and VOR. The patients with focal neurologic signs, abnormal hearing, caloric paresis or acute lesion on brain imaging were excluded. RESULTS: Positional downbeat nystagmus was developed during lying down, straight head-hanging and/or Dix-Hallpike position. Perverted head-shaking nystagmus was observed in seven patients (58.3%). Gait disturbance revealed in six patients. Other cerebellar manifestations including saccadic dysmetria and gaze-evoked nystagmus were not observed. The gains of VOR were increased than normal controls. However, the gains of visual enhancement and visual cancellation of the VOR were not different from controls and OKN/OKAN were normal. The mean VOR time constants did not differ between patients and normal controls. However, tilt suppression of the post-rotatory nystagmus was impaired in the patients (p<0.01). All patients showed normal findings in head thrust test, caloric response, BAEPs, and brain imaging. CONCLUSION: Isolated positional downbeat nystagmus (pDBN) in patients complained intermittent dizziness showed frequently accompanied perverted head-shaking nystagmus (HSN) and increased gain of VOR and impaired tilt suppression. This finding tells us that isolated positional downbeat nystagmus (pDBN) reflects pathologic central nystagmus results from cerebellar (uvulonodular) dysfunction.
